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CLINICAL    CAKDIOLOGY 


•The 


THE  MACMILLAN  COMPANY 

NEW  YORK    •    BOSTON   •    CHICAGO    •    DALLAS 
ATLANTA   -    SAN    FRANCISCO 

MACMILLAN  &  CO.,  Limited 

LONDON    •    BOMBAY   •    CALCUTTA 
MELBOURNE 

THE  MACMILLAN  CO.  OF  CANADA,  Ltd. 

TORONTO 


CLINICAL  CARDIOLOGY 


BY 


SELIAN   NEUHOF,  B.S.,  M.D. 

VISITING    PHYSICIAN,    CENTRAL   AND   NEUROLOGICAL   HOSPITAL 
ADJUNCT    ATTENDING    PHYSICIAN,    LEBANON   HOSPITAL 


THE    MACMILLAN    COMPANY 

1917 

All  rights  reserved 


Copyright,  1917, 
By  THE  MACMILLAN  COMPANY. 


Set  up  and  electrotyped.     Published  September,  1917. 


Nortaooo  ^reas 

J.  S.  Cushing  Co.  —  Berwick  &  Smith  Co. 

Norwood,  Mass.,  U.S.A. 


TO 

i 

MY  PARENTS 

IN    TRIBUTE    TO    THEIR    CONSTANT    SELF- 
SACRIFICE,    THIS    BOOK 
IS    AFFECTIONATELY   DEDICATED 


PREFACE 

In  the  many  recent  books  on  cardiac  disease,  dealing  chiefly  with 
polygraphy,  electrocardiography,  and  orthodiascopy,  there  has  been 
much  confusion  regarding  the  proportionate  value  of  graphic  methods, 
with  the  result  that  undue  emphasis  has  been  placed  upon  purely  in- 
strumental and  technical  considerations.  The  author  has,  therefore, 
included  in  this  book  the  graphic  as  well  as  the  usual  bedside  methods, 
while  writing  from  the  clinician's,  rather  than  from  the  cardiologist's 
standpoint,  and  he  believes  that  this  work  will  therefore  supply  a  com- 
prehensive,, practical  reference  book  for  both  practitioner  and  student. 

The  opening  chapters  are  devoted  to  a  description  of  instrumental 
and  graphic  methods  in  the  study  and  examination  of  normal  and 
abnormal  rhythms  and  of  normal  and  abnormal  silhouettes.  From  a 
study  of  these  chapters,  the  physician  is  enabled  to  discern  the  rela- 
tion and  application  of  instrumental  methods  to  clinical  cardiology  and 
bedside  examination.  Without  minimizing  their  importance,  I  have 
emphasized  the  fact  that  instrumental  methods  are  not  infrequently 
subsidiary.  Indeed,  as  will  be  shown,  graphic  devices  may  sometimes 
be  dispensed  with  if  their  fundamental  significance  is  comprehended. 

Subsequent  chapters  are  devoted  to  the  purely  clinical  side  of  cardi- 
ology. Careful  consideration  is  given  to  the  important  subjects  of  the 
pathology,  etiology,  diagnosis,  prognosis,  and  therapy  of  endocarditis, 
myocarditis,  and  cardiosclerosis.  Questions  occurring  in  everyday 
practice  with  reference  to  diet,  exercise,  and  general  management  of 
heart  disease  are  fully  dealt  with.  There  are  special  chapters  on  pre- 
cordial pains,  blood  pressure,  and  the  heart  in  pneumonia. 

I  desire  to  express  my  sincere  thanks  to  Dr.  Alfred  E.  Cohn  of  the 
Rockefeller  Institute  for  valuable  aid  and  suggestions,  especially  on 
the  chapters  dealing  with  the  arrhythmias ;  to  my  publishers,  The  Mac- 
millan  Company,  for  courteous  cooperation ;  and  to  my  wife,  without 
whose  aid  and  stimulus  this  book  could  not  have  been  written. 


Vll 


CONTENTS 

PAGE 

Chapter  I.     The  Heart 1 

Its  Development  —  Position  in  the  Chest  —  Anatomy  and  Physi- 
ology —  Nerve,  Lymphatic,  and  Arterial  Supply. 

Chapter  II.     The  Conduction  System 7 

Position  and  Structure  of  the  Pacemaker  —  Nerve  and  Arterial 
Supply  —  Position,  Distribution,  Dissection,  and  Structure  of  the 
Auriculo-ventricular  Conduction  System  —  Course  of  the  Normal 
Impulse  —  Neurogenic  or  Myogenic  Impulse  ? 

Chapter  III.     Polygraphic  Tracings 12 

Mackenzie  Polygraph  —  Venous  Pressure  Curves  —  Schematic 
Curves  —  Phlebogram  —  Physiological  Variations  —  Dicrotic  Wave 

—  Types  of  Pulse  —  Radial  Palpation. 

Chapter  IV.     The  Electrocardiogram 22 

Fundamental  Physiological  Considerations  —  Electrocardiographic 
Apparatus  —  Methods  of  Taking  the  Electrocardiogram  —  The 
Three  Leads  —  Normal  Electrocardiogram  —  Its  Interpretation  — 
Normal  and  Abnormal  Electrocardiograms  —  Variations  Due  to 
Change  of  the  Ventricular  Axis  —  Squatty,  Vertical,  and  Drop  Hearts 

—  Shift  of  the  Interventricular  Septum  —  Ventricular  Hypertrophy 
and  Dilatation  —  Congenital  Dextrocardia  —  Phasic  Variation  with 
Breathing  —  Different  Positions  of  the  Heart  in  the  Chest  —  Intra- 
ventricular Block  —  Abnormally  Wide  R. 

Chapter  V.         Mathematical     Considerations     Underlying     the 

Electrocardiogram  .         .         .         .         .         .      •   .         .         .39 

"  Manifest"  Size  —  Angles  Produced  by  the  Leads  with  the  Electri- 
cal Axis  —  Their  Mathematical  Measurement  and  Approximation. 

Chapter  VI.     Course  of  the  Excitation  Wave  ....       44 

Effect  of  Vagus  and  Accelerator  Stimulation  upon  the  Electro- 
cardiogram. 

T  Wave  :  Its  Variations  and  Clinical  Significance. 

Chapter  VII.     The    Arrhythmias  —  Their    Polygraphic,    Electro- 
cardiographic, and  Clinical  Recognition    .....       47 

Tabulation  —  Auricular  Arrhythmias  —  Ventricular  Arrhythmias  — 
True  Bradycardia  —  Arrhythmias  from   Disturbances  in  the  Sino- 
auricular  and  the  Atrio-ventricular  Nodes. 
Alternation  —  Pulsus  Paradoxus. 

ix 


x  CONTENTS 

PAGE 

Chapter  VIII.     The  Arrhythmias,  Their  Etiology  and  Therapy    .       96 
General       Considerations  —  Sinus      Arrhythmia  —  Sino-auricular 
Block  —  Extras  y stoles  —  True  Bradycardia. 

Heart  Block  :    Etiology  —  Cardiac   Disease  —  Drugs  —  Asphyxia 

—  Chemical  Poisons  —  Interference  with  Cerebral  Circulation  — 
Abnormal  Pressure  on  the  Cardio-inhibitory  Center  —  Abnormal 
Pressure  on  the  Vagus  — ■  Increased  Vagal  Inhibition  by  Digital 
Pressure,  and  by  Reflex  Peripheral  Excitation. 

Prolonged  Conduction  Time  —  Shortened  Conduction  Time  — 
Auricular  Fibrillation  —  Simple  Tachycardia  —  Paroxysmal  Tachy- 
cardia —  Auricular  Flutter  —  Ventricular  Escape. 

Chapter  IX.     Orthodiascopy  and  Fluoroscopy  ....     110 

Their  Advantages  —  Description  of  the  Orthodiascopic  Apparatus 

—  Its  Use  Combined  with  Fluoroscopy  —  Normal  Orthodiascopic 
Tracing  —  Its  Measurement  —  Objections  to  Measurement  as  a 
Standard  —  Abnormally  Broad  and  Abnormally  Slender  Hearts  — 
Orthodiagrams  and  Fluoroscopy  in  Mitral  and  Aortic  Valvular 
Lesions  —  Aortitis  Involving  the  First  Portion,  Arch  and  Descending 
Thoracic  Aorta  —  Congenital  Cardiac  Malformations  of  the  Aorta  — 
Patent  Ductus  Arteriosus  —  Patent  Interventricular  Septum  —  Pat- 
ent Foramen  Ovale. 

Chapter  X.     Physical  Examination  of  the  Heart  .         .         .     129 

Inspection  —  Palpation  —  Percussion  —  Rational  Method  for  the 
Determination  of  the  Cardiac  Outline  —  Auscultation  —  Valvular 
Murmurs  —  Murmurs  in  Atherosclerosis  —  Non-organic  "  Func- 
tional" Murmurs  of  Intracardiac  Origin  —  Third  Heart  Sound  — 
Extracardiac  Inorganic  Murmurs  —  Cardio-respiratory  and  Cardio- 
pulmonary Murmurs  —  Reduplicated  Sounds  —  Reduplicated  Apical 
Impulse  —  Reduplicated  First  and  Second  Sounds. 

Chapter  XI.      Etiology  of    Endocarditis  and  of    Cardiovascular 

Disease 149 

Classification  —  Chemical  Agents  —  Metallic  Poisons  —  Lead  — 
Alcohol  —  Tobacco  :  Experimental  Observations,  Neurotropic  Ac- 
tion —  Diabetes  —  Gout  —  Food  Metabolism  :  Experimental  and 
Clinical  Evidence  —  Bacterial  Toxins  —  Diphtheria  :  Myocardial 
Changes,  Heart  Block,  Milder  Toxemia,  Arrhythmias,  Unexpected 
Death  —  Pneumonia  —  Heart  Block  in  Pneumonia,  Effect  of  Pneu- 
monia on  the  Heart  Muscle,  Experimental  Evidence,  Cardiovascular 
Disease  as  a  Late  Sequela  —  Rheumatism  and  Tonsillitis  —  Relation 
between  Rheumatism  and  Tonsillitis  —  Pyorrhea  Alveolaris  —  Strepto- 
coccus Viridans  in  the  Mouth  —  Pyogenic  Abscesses  —  Bacterial  Endo- 
carditis :  Its  Relation  to  Rheumatism  —  Classification  of  Organisms  : 
Their  Frequency  —  Frequency  of  Affections  of  the  Various  Valves  — 
Streptococcus  Viridans  —  Renal  Infarction  —  Distinction  between 
Acute  and  Chronic  Streptococcus  Viridans  —  Spirochetal  Infection  — 
Syphilis:  Pathological  Changes,  Wassermann  Reaction. 


CONTENTS  xi 


Chapter  XII.      Pathology  of  the  Endocardium  and  Myocardium  — 

Pathology  of  Cardiosclerosis        .......     160 

Chapter  XIII.  Symptomatology,  Therapy,  and  Prognosis  of  Rheu- 
matic Endocarditis 165 

Clinical  Phenomena  and  Signs  of  Acute  Rheumatic  Endocarditis  — 
Endocardial  Exacerbations  —  Clinical  Phenomena  of  Chronic  Rheu- 
matic Endocarditis  —  Decompensation  —  Types  of  Dyspnoea  — 
"Acidosis  "  —  Cyanosis  —  Visceral  Congestion  —  Special  Signs  and 
Symptoms  of  Decompensation  in  the  Various  Valvular  Lesions  — 
Paralysis  of  the  Left  Recurrent  Laryngeal  in  Mitral  Stenosis  — - 
Therapy  in  Acute  and  Chronic  Rheumatic  Endocarditis  — •  Prognosis 
in  Acute  and  Subacute,  Quiescent,  and  Chronic  Stages. 

Acute  Bacterial  Endocarditis 176 

Symptomatology  —  Therapy. 
Subacute    and    Chronic    Streptococcus    Viridans     Infection. 

Pathology  —  Clinical  Course  —  Petechias  —  Heubner's  Nodes  — 
Skin  Gangrene  —  Hematology  —  Renal  Manifestations  —  Neuro- 
logical Manifestations  —  Cardiac  Manifestations  —  Blood  Culture 
—  Bacteria-free  Stage  — ■  Therapy. 

Chapter  XIV.     Cardiac  Syphilis  .......     184 

The  Heart  in  Secondary  and  Tertiary  Syphilis  —  Myocarditis  — 
Aortitis. 

Physical  Signs  of  Aneurismal  Dilatation  of  the  First  Portion  and 
Arch  of  the  Aorta  —  Diagnosis,  Symptomatology,  Prognosis,  and 
Therapy  of  Dilatation  Aneurisms  of  the  Descending  Thoracic  Aorta. 

Chapter  XV.  Symptomatology,  Physical  Signs,  Diagnosis  and 
Prognosis  of  Myocarditis  and  Cardiosclerosis  —  Physical 
Signs  and  Diagnosis  of  Ventricular  Hypertrophy    .         .         .     194 

Chapter  XVI.  Therapy  in  Circulatory  Disease  ....  206 
Digitalis :  General  Considerations,  Use  in  Auricular  Fibrillation 
and  Other  Arrhythmias,  Arrhythmias  Produced  by  Digitalis,  Cause  of 
Digitalis  Vomiting  and  Its  Prevention  —  Preparations  and  Dosage, 
Coupled  Rhythm  and  Digitalis,  Use  of  Digitalis  in  Decompensation 
with  Regular  Pulse,  Cumulative  Effect,  Continuance  of  the  Effect  of 
the  Drug,  Possible  Dangers,  Other  Therapeutic  Indications,  Sum- 
mary and  Conclusions. 

Tincture  Strophanthus  :  Strophanthin  —  Squills  —  Apocynum  — 
Caffeine  and  Its  Derivatives :     Theobromin  Sodium  Salicylate. 

Karrell  Diet :  Its  Use,  Indications,  and  Modification  —  Strych- 
nine —  Nitrite  Group  —  Camphor  — Alcohol  —  Aconite  —  Spartein  — 
Adrenalin  —  Sedatives  —  Acetate  of  Potash  and  Sodium  —  Purging 
Salts  —  Calomel  —  Venesection  —  Vaccines  —  Sera  —  Silver  Prepa- 
rations —  Massage  —  Passive  Motion  —  Calisthenics  —  Medical  Gym- 
nastics —  Resistance  Exercises  —  Walking  —  Hydrotherapy  —  Baths  : 
Carbonated  and  Oxygenated  Baths  —  Tonsillectomy  —  Extraction  of 
Teeth. 


xii  CONTENTS 

PAGE 

Chapter  XVII.  Diet,  Renal  and  Blood  Tests  in  Cardiac  Disease  229 
General  Considerations  —  Diet  in  Compensated  Endocarditis  —  In 
Obese  Individuals  —  In  Myocardial  Insufficiency  with  and  without 
Edema  —  Tests  for  Renal  Insufficiency  :  Phenolsulphophthalein 
Test :  Method  of  Administration,  Conclusions  —  Nephritic  Test  Diets 
— Estimation  of  Water,  Salt,  and  Urea  Output  in  the  Urine  —  Chemi- 
cal Examination  of  the  Blood :  Non-protein  Nitrogen  —  Diet  in 
Cardiosclerosis  and  Nephritis  —  Sugar  Solution  and  Bicarbonate  of 
Soda  in  Nephritis. 

Chapter  XVIII.     Management  of  Cardiac  Disease  .         .         .     235 

Fundamental  Considerations  —  Types  of  Exercise  and  Occupation 
—  Functional  Efficiency  Tests  —  Indications  for  Drug  Therapy. 

Marriage  in  Women  with  Valvular  Lesions       ....     237 

General  Considerations.  Cardiac  Symptoms  during  Gestation  — 
Prognostic  Consideration  of  the  Various  Valvular  Lesions,  Indications 
for  Terminating  Pregnancy. 

Chapter  XIX.     Blood  Pressure 242 

Physiological  Considerations ;  Factors  Involved,  Cardiac  Energy, 
Peripheral  Resistance,  Elasticity  of  Arterial  Walls,  Volume  of  Cir- 
culating Blood,  Viscosity  of  Blood  —  Clinical  Estimation  of  Blood 
Pressure  —  Types  of  Instruments  —  Methods  of  Blood  Pressure 
Estimation  :  Auscultatory  Method  and  Its  "  Phases  "  —  Normal 
Blood  Pressure :  Physiological  Variations  —  Effect  of  Alcohol, 
Excitement,  Cyanosis,  Smoking  —  Increased  Intracranial  Pressure  — 
Hypertonus  —  Clinical  Classification  for  Study  of  Blood  Pressure  — 
Hypertensive  Cardiovascular  Disease  with  Myocarditis  —  Hyper- 
tension and  Myocardial  Insufficiency  with  Labile  Vasomotor  Mecha- 
nism —  Uremic  Group  —  Myocardial  Disease  and  Insufficiency 
without  Hypertension  —  Valvular  Disease  and  Myocardial  Insuffi- 
ciency with  and  without  Hypertension  —  Hypotension  —  Blood 
Pressure  in  Cardiac  Arrhythmias  —  Therapeutics  of  Hypertension : 
Vasodilators,  Venesection,  Hydrotherapy,  Diathermy,  Diet,  Exercise. 

Chapter  XX.     "Weak"  Heart 255 

Clinical  Symptoms  —  Illustrative  Cases  —  Therapy. 

Chapter  XXI.     Precordial  Pains   of    Cardiovascular  and  Extra- 
cardiac  Origin  —  Angina  Pectoris 258 

Historical  —  Confusion  of  Terms  —  Cardiovascular  Nerve  Sup- 
ply —  Epigastric  Pains  and  Heart  Disease  —  Intra-  and  Extra-cardiac 
Disease  —  Classification  of  Common  Causes  of  Precordial  Pain  — 
Organic  Cardiovascular  Disease :  Illustrative  Cases  —  Extracar- 
diac  Disease  :  Illustrative  Cases. 

Chapter  XXII.     Therapy    of    Pneumonia    from    the    Circulatory 

Standpoint 273 


LIST   OF   PLATES 


Plate  I 

Plate  II 

Plate  III 

Plate  IV 


Plate        V  — 


Plate      VI 


Plate    VII  — 


Plate  VIII  — 


Plate      IX 


Fig.  7 
Fig.  32 
Fig.  33 
Fig.  36 
Fig.  39 
Fig.  40 
Fig.  41 
Fig.  42 
Fig.  45 
Fig.  47 
Fig.  48 
Fig.  49 
Fig.  50 
Fig.  51 
Fig.  52 
Fig.  53 
Fig.  54 
Fig.  55 
Fig.  56 
Fig.  59 
Fig.  60 
Fig.  61 
Fig.  62 
Fig.  63 
Fig.  65 
Fig.  66 
Fig.  67 
Fig.  68 
Fig.  69 
Fig.  73 
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Fig.  75 
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Fig.  95 
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XIV 

Plate     X 
Plate    XI 


Plate   XII 
Plate   XIII 


Plate      XIV  — 


LIST    OF   PLATES 


Plate 


XV 


Plate  XVI 

Plate  XVII 

Plate  XVIII 

Plate  XIX 

Plate  XX 


Fig.  99 
Fig.  130 
Fig.  131 
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COMPLETE  LIST   OF   ILLUSTRATIONS 

Fig. 

1  —  Heart  of  the  human  embryo. 

2  —  Diagrammatic  position  of  the  cardiac  valves. 

3  —  Schematic  view  of  sino-aucurilar  node  of  dog. 

4  —  Detail  of  the  S-A  node  of  dog. 

5  —  Right   ventricle   of   ox  heart,   showing   the   auriculo-ventricular   node 

(A-V  node)  and  the  main  stem. 

6  —  Left  ventricle  of  ox  heart,  showing  conduction  system. 

7  —  Plate  I  —  Mackenzie  Ink  Polygraph. 

8  —  Schematic  view  of  the  a-c-v  waves  and  of  the  jugular  bulb. 

9  —  Diagrammatic  representation  of  the  normal  polygraphia  curve. 
10  —  Normal  venous  and  radial  tracing. 

11-13  —  Split  c(c-c)  waves  in  the  venous  tracing. 

14  —  Combined  venous  and  arterial  tracing  in  the  jugular. 

15-16  —  h  wave  in  the  jugular  tracing. 

17  —  Normal  phlebogram  in  aortic  regurgitation. 

18-19  —  Normal  jugular  tracing  in  aortic  stenosis  and  double  mitral  lesion. 

20  —  Normal  a  and  other  peaks  in  mitral  stenosis. 

21  —  Normal  a  wave  in  mitral  regurgitation. 

22-25  —  Normal  jugular  tracings  in  exophthalmic  goiter. 

26  —  Normal  radial  pulse  tracing. 

27  —  Low  dicrotic  notch  in  aortic  regurgitation. 

28  —  Low  dicrotic  notch  in  aortic  aneurism. 

29  —  Scheme  of  monophasic  action  current. 

30  —  Scheme  of  diphasic  action  current. 

31  —  Scheme  of  rheostat  and  connection  with  the  galvanometer. 

32  —  Plate  II  —  Photograph     of    the    Electrocardiographic    Apparatus    in 

Position. 

33  —  Plate  III  —  Photograph  of  patient  with  electrodes  cbnnected  with  the 

galvanometer. 

34  —  Diagram  illustrating  the  three  leads. 

35  —  Schematic  representation  of  a  typical  electrocardiogram. 

36  —  Plate  IV  —  Electrocardiogram  showing  the  deflection  time  of  the  string. 

37  —  Normal  electrocardiogram. 

38  —  Scheme  showing  the  angles  made  by  the  leads  with  the  varying  ven- 

tricular axes. 

39  —  Plate  IV  —  Electrocardiogram  of  normal  patient ;  negative  R  in  L  III. 

40  —  Plate  IV  —  Electrocardiogram  of  normal  patient ;  negative  R  in  L  III. 

41  —  Plate  IV  —  Electrocardiogram  of  normal  patient ;  negative  R  in  L  III. 

XV 


xvi  COMPLETE   LIST    OF   ILLUSTRATIONS 

Fig. 

42  —  Plate  V  —  Electrocardiogram  of  patient  with  narrow  heart. 

43  —  Orthodiascope  tracing  of  heart  of  normal  child  lying  on  its  back  (A), 

left  (B)  and  right  (C)  sides. 

44  —  Orthodiascopic  tracing  of  heart  of  normal  child  lying  on  its  back  (A), 

left  (B)  and  right  (C)  sides. 

45  —  Plate  V  —  Electrocardiogram  of  a  child  whose  orthodiascopic  tracing  is 

Fig.  148. 

46  —  Electrocardiogram  of  congenital  dextrocardia. 

47  —  Plate  V  —  Electrocardiogram  of  acquired  dextrocardia. 

48-49  —  Plate  V  —  Electrocardiogram  showing  slight  respiratory  phasic  varia- 
tion. 

50  —  Plate  VI  —  Electrocardiogram  of  marked  respiratory  phasic  variation. 

51  —  Plate  VI  —  Electrocardiogram  of  aneurismal  dilatation  of  the  aorta  and 

left  ventricular  hypertrophy. 

52  —  Plate  VI  —  Electrocardiogram  of  aortic  stenosis  and  left  ventricular 

hypertrophy. 

53  —  Plate  VI  —  Electrocardiogram  of  left  ventricular  hypertrophy. 

54  —  Plate  VI  —  Electrocardiogram  of  aortic  regurgitation  and  left  ventric- 

ular hypertrophy. 

55  —  Plate  VI  —  Electrocardiogram  of  congenital  ductus  arteriosus. 

56  —  Plate  VII  —  Electrocardiogram   showing    an   interpolated   extrasystole 

and  an  abnormally  wide  R. 

57  —  Electrocardiogram  of  advanced  mitral  stenosis  and  auricular  fibrillation. 

58  —  Electrocardiogram  of  advanced  mitral  stenosis  and  auricular  fibrillation. 

59  —  Plate  VII  —  Electrocardiogram  of  thickened  R  summit. 

60  —  Plate  VII  —  Electrocardiogram  of  notched  R  summit. 

61  —  Plate  VII  —  Electrocardiogram  of  split  R  (M  complex). 

62  —  Plate  VII  —  Electrocardiogram  of  split  R  {W  complex). 

63  —  Plate  VII  —  Electrocardiogram  of  split  R  (W  complex). 

64  —  Electrocardiogram  of  notched  P  wave  in  mitral  stenosis. 

65  —  Plate  VII  —  Electrocardiogram  of  intraventricular  block. 

66  —  Plate  VII  —  Electrocardiogram  of  ventricular  complexes  of  abnormal 

width  and  normal  form. 
67-69  —  Plate  VIII  —  Electrocardiograms  of  ventricular  complexes  of  abnor- 
mal width  and  normal  form. 
70-71  —  Diagrams  of  relation  of  the  ventricular  axis  to  the  leads. 

72  —  Diagram  of  the  direction  of  the  leads  to  the  electrical  axes. 

73  —  Plate  VIII  -^  Electrocardiogram  showing  tall  T  II. 

74  —  Plate  VIII  —  Electrocardiogram  showing  T  taller  than  R. 

75  —  Plate  VIII  —  Electrocardiogram  showing  negative  T  III. 

76  —  Plate  IX  —  Electrocardiogram  showing  diphasic  T  II  and  negative  T  II 

and  T  III. 
77-82  —  Diagrams  showing  the  origin  of  physiological  and  pathological  con- 
tractions. 
83-87  —  Polygrams  of  ventricular  extrasystoles. 


COMPLETE    LIST    OF   ILLUSTRATIONS  xvii 

Fio. 

88-92  —  Polygrams  of  auricular  extrasystoles. 

93-94  —  Polygrams  of  multiple  auricular  extrasystoles. 

95-98  —  Plate  IX  —  Electrocardiograms  of  auricular  extrasystoles. 

99  —  Plate  X  —  Electrocardiogram  of  auricular  extrasystoles   coming  from 

two  ectopic  foci. 
100-101  —  Polygrams  of  varying  ventricular  rates  in  exophthalmic  goiter. 
102  —  Polygram  of  paroxysmal  tachycardia. 
103-106  —  Polygrams  of  exophthalmic  goiter. 
107-120  —  Polygrams  of  various  types  of  auricular  fibrillation. 

121  —  Polygram  of  auricular  fibrillation  with  anacrotic  radial  pulse. 

122  —  Polygram  of  auricular  fibrillation  and  fibrillary  (/)  waves. 

123  —  Polygram  of  auricular  fibrillation. 

124  —  Polygram  of  auricular  fibrillation  with  rhythmical  radial  pulse. 
125-129  —  Arteriograms  of  auricular  fibrillation  illustrating  pulse  irregularities. 

130  —  Plate  X  —  Electrocardiogram  showing  small,  fairly  regular  fibrillation 

waves. 

131  —  Plate  X  —  Electrocardiogram  showing  very  fine  fibrillation  waves. 

132  —  Plate  XI  —  Electrocardiogram  showing  fairly  regular  fibrillation  waves 

resembling  flutter.     • 

133  —  Electrocardiogram  with  fine  fibrillation  waves. 

134  —  Plate  XI  —  Electrocardiogram  with  various  types  of  fibrillation  waves. 

135  —  Plate  XI  —  Electrocardiogram  with  very  fine  fibrillation  waves. 

136  —  Electrocardiogram  with  fairly  regular  fibrillation  waves. 

137  —  Electrocardiogram  of  auricular  fibrillation  showing  tachycardia. 

138  —  Electrocardiogram  of  auricular  fibrillation  with  ectopic  beats. 

139  —  Electrocardiogram  of  auricular  fibrillation  with  coarse  waves. 

140  —  Electrocardiogram  of  auricular  and  ventricular  extrasystoles,  and  auric- 

ular fibrillation. 
141-143  —  Polygrams  of  auricular  flutter. 

144  —  Plate  XIII  —  Electrocardiogram  of  auricular  flutter ;  incomplete  heart 

block  (4:1). 

145  —  Electrocardiogram  of  paroxysmal  auricular  tachycardia  and  auricular 

fibrillation. 

146  —  Electrocardiogram  of  nodal  extrasystole. 
147-148  —  Polygrams  of  nodal  extrasystoles. 

149-150  —  Polygrams  of  ventricular  extrasystoles  with  compensatory  pauses. 
151  —  Polygram  of  ventricular  extrasystole  with  decreased  compensatory  pause. 
152-153  —  Polygrams  of  ventricular  extrasystoles  without  compensatory  pauses. 

154  —  Schematic  view  of  types  of  ventricular  extrasystole  showing  the  direc- 

tion of  the  corresponding  R  deviations. 

155  —  Electrocardiogram  of  ventricular  extrasystole  from  right  ventricle  near 

the  base. 

156  —  Electrocardiogram  of  ventricular  extrasystole  from  left  ventricle  near 

the  base. 

157  —  Electrocardiogram  of  ventricular  extrasystole  from  wall  of  left  ventricle. 


xviii  COMPLETE   LIST   OF   ILLUSTRATIONS 

Fig. 

158  —  Electrocardiogram   of   extrasystoles   arising   from   various    ventricular 

foci,  with  complete  heart  block. 

159  —  Electrocardiogram  of  coupled  rhythm  (pulsus  bigeminus). 

159  A-159  B  —  Polygram  of  frustrate  ventricular  extrasystoles  (coupled  rhythm) . 

160  —  Electrocardiogram  of  paroxysmal  tachycardia  of  ventricular  origin. 

161  —  Polygram  of  ventricular  escape. 

162  —  Plate  XIV  —  Electrocardiogram  of  ventricular  escape. 

163  —  Plate  XIII  — Electrocardiogram  of  lesion  of  the  left  branch  of  the   con- 

duction system. 

164  —  Electrocardiogram  of  lesion  of  the  right  branch  of  the  conduction  system. 
165-168  —  Polygrams  of  true  bradycardia. 

169  —  Plate  XIV  —  Electrocardiogram  of  true  bradycardia. 
170-171  —  Arteriograms  of  sinus  arrhythmia. 

172  —  Arteriogram  of  sinus  slowing. 

173  —  Arteriogram  of  slight  sinus  arrhythmia. 
174-175  —  Polygrams  of  sinus  arrhythmia. 

176  —  Polygram  of  sinus  arrhythmia,  non-respiratory  type. 

177  —  Electrocardiogram  of  sinus  arrhythmia  of  respiratory  origin. 

178  —  Electrocardiogram  of  sino-auricular  block  due  to  smoking. 

179  —  Plate  XV  —  Electrocardiogram  of  sino-auricular  block. 

180  —  Diagram  showing  the  effect  of  nicotine  upon  the  vagus  and  accelerators. 

181  —  Electrocardiogram  of  blocked  auricular  beat. 

182  —  Electrocardiogram    showing  very  slow  ventricular  rate  and  .prolonged 

P-R  time. 

183  —  Plate  XIV  —  Electrocardiogram  of  prolonged  conduction  time. 

184  —  Electrocardiogram  of  backward  conduction  from  ventricle  to  auricle. 

185  —  Polygram  of  incomplete  block. 

186  —  Polygram  of  incomplete  block  and  ventricular  extrasystole. 
187-192  —  Polygrams  of  complete  heart  block. 

193  —  Polygram  of  complete  heart  block  and  irregular  ventricular  action. 

194  —  Polygram  of  complete  heart  block  and  ventricular  extrasystole. 

195  A  and  B  : —  Polygrams  of  heart  block,  ectopic  beats  and  auricular  fibrillation. 

196  A  and  B  —  Polygrams  of  prolonged  conduction  time  and  heart  block. 

197  —  Electrocardiogram  of  complete  heart  block. 

198  —  Electrocardiogram  of  incomplete  and  complete  heart  block. 

199  —  Arteriogram  showing  slight  alternation. 

200-201  —  Arteriograms  of  alternation  following  extrasystoles. 

202  —  Plate  XVII  —  Groedel  Apparatus. 

203  —  Plate  XVIII  —  Details  of  marking  mechanism  of  Groedel  apparatus. 

204  —  Orthodiascopic  tracing  of  normal  heart. 

205  —  Orthodiascopic  tracing  of  long  and  slender  heart. 

206  —  Copy  of  an  orthodiascopic  tracing  of  a  broad  heart. 

207-208  —  Orthodiascopic   tracings    of    abnormally    slender    hearts     ('drop' 

hearts) . 
209  —  Orthodiascopic  tracing  of  compensated  mitral  regurgitant  lesion. 


COMPLETE    LIST    OF   ILLUSTRATIONS  xix 

Fig. 

210  —  Orthodiagram  of  compensated  double  mitral  lesion. 

211-213  —  Orthodiagrams  of  globular  hearts  of  cases  of  decompensated  double 

mitral  lesions  with  auricular  fibrillation. 
214  —  Orthodiagram  of  globular  heart  of  extreme  size. 
215-216  —  Orthodiascope  tracings  of  slightly  globular  hearts  with   moderate 

enlargement. 

217  —  Orthodiagram  of  extreme,  rounded  right-sided  enlargement. 

218  —  Orthodiascope  tracing  of  double  mitral  lesion. 

219  —  Orthodiascope  tracing  of  recent  mitral  regurgitant  lesion. 

220  —  Orthodiagram  of  mitral  regurgitant  lesion  showing  a  somewhat  ovoid 

contour. 

221  —  Orthodiagram  of  old  rheumatic  double  aortic  lesion. 

222  —  Orthodiagram  of  aortic  regurgitation. 

223-224  —  Orthodiagrams  of  double  mitral  and  aortic  lesions. 

225  —  Orthodiagram  of  dilatation  of  aortic  arch  with  left  ventricular  hyper- 

trophy. 

226  —  Orthodiagram  of  aortitis. 

227  —  Orthodiagram  of  dilatation  of  aortic  arch  and  left  ventricular  hyper- 

trophy. 

228  —  Orthodiagram  of  aortitis  of  first  portion  and  arch  of  the  aorta,  and 

extreme  left  ventricular  hypertrophy. 

229  —  Orthodiagram  of  luetic  aortitis  and  left  ventricular  hypertrophy. 

230  —  Orthodiagram  of  enlargement  and  low  implantation  of  the  first  portion 

of  the  aorta,  and  moderate  enlargement  of  the  left  ventricle. 

231  —  Orthodiagram  of  luetic  aortitis  and  left  ventricular  hypertrophy. 

232  —  Orthodiagram  of  diffuse  aneurismal  dilatation  of  the  descending  thoracic 

aorta. 

233  —  Plate  XIX  —  Photograph  from  X-ray  plate,  showing  aneurismal  dila- 

tation of  the  descending  thoracic  aorta. 

234  —  Plate  XX  —  Photograph  from  Roentgenogram  of  aneurismal  dilatation 

of  the  descending  thoracic  aorta. 

235  —  Orthodiagram  of  aneurismal  dilatation  of  the  arch  and  descending  thoracic 

aorta. 

236  —  Orthodiagram  of  aneurism  of  the  first  portion  of  the  aorta  due  to  con- 

genital aortic  stenosis. 

237  —  Orthodiagram  of  double  mitral  lesion  and  aortic  aneurism. 

238  —  Orthodiagram  of  patent  ductus  arteriosus. 

239  —  Orthodiagram  of  congenital  dextrocardia  and  patent  interventricular 

septum. 

240  —  Diagram  of  probable  cardiac  circulation  in  patent  interventricular  septum. 

241  —  Outline  of  heart  with  dilated  right  auricle. 

242-246  —  Diagrams  of  difference  in  percussion  and  orthodiascope  outlines  of 

normal  and  abnormal  hearts. 
247  —  Orthodiascope  tracing  from  a  case  of  mitral  stenosis  and  left  recurrent 
laryngeal  paralysis. 


\L£FT 


CLINICAL    CARDIOLOGY 


CHAPTER  I 
THE   HEART 

Development  of  the  Heart.  —  In  very  early  fetal  life  the  heart  is 
represented  by  a  simple  tube,  the  cardiac  tube.  It  consists  of  two  dis- 
tinct strata :  an  inner,  thinner  layer,  derived  from  the  hypoblast,  which 
later  becomes  the  endocardium ;  and  an  outer,  thicker  layer,  derived  from 
the  visceral  mesoblast,  which  finally  develops  into  the  musculature. 
Later,  the  cardiac  tube  elongates  and  becomes  bent  upon  itself  so  as 
to  form  an  S-shaped  loop,  with  an  anterior  right,  and  a  posterior  left 
angle.  Slight  constrictions  soon  appear,  which  serve  to  divide  the  loop 
into  four  parts  (Fig.  1)  :  (1)  the  sinus  venosus  (sinus  reuniens  of  His), 
(2)  the  common  auricle,  (3)  the  common  ven- 
tricle, (4)  the  aortic  bulb.  The  sinus  venosus 
is  at  first  situated  transversely  behind  the  com- 
mon auricle  and  connects  with  the  latter  by  a 
median  aperture  ;  it  afterwards  becomes  oblique 
and  divides  into  two  projections  or  horns:  the  ev' 
right  forms  part  of  the  right  auricle,  the  line  of  FiG  1>_Heartcf  thehu- 
union  being  marked  in  the  adult  heart  by  a  ver-  man  embryo  5  mm.  long. 
tical  crest,  the  crista  terminalis  of  His;  the  left  (Modified  from  His.) 
horn  persists  as  the  coronary  sinus.  The  com- 
mon auricle  (C.A)  becomes  partitioned  off  into  right  and  left  auricles 
by  the  gradual  formation  of  a  septal  wall,  the  septum  superius ;  the 
foramen  ovale  results  from  a  perforation  of  this  wall.  Another  sep- 
tal structure,  the  septum  inferius,  similarly  forms,  and  separates^  the 
common  ventricle  {C.V)  into  right  and  left  chambers.  For  some  time, 
however,  it  does  not  quite  reach  the  auricular  canal,  thus  leaving  a 
foramen  between  the  auricles  and  ventricles,  the  common  auric- 
ulo-ventricular  orifice.  The  formation  of  a  septum  is  also  responsible 
for  the  division  of  the  aortic  bulb  (A.B)  into  the  two  great  vessels, 
—  the  aorta  and  the  pulmonary  artery. 

Position  of  the  Fetal  Heart.  —  In  early  fetal  life,  the  heart  lies  im- 
mediately under  the  head  and  is  of  relatively  large  size.  Later,  it  be- 
comes a  thoracic  organ,  lying  at  first  vertically,  then  gradually  assuming 

B  1 


CLINICAL   CARDIOLOGY 


a  more  oblique  position.  The  auricular  portion  with  its  intercommunica- 
tion (the  foramen  ovale)  is  at  first  larger  than  the  ventricle.  By  means 
of  the  ductus  arteriosus  (ductus  Botalli),  the  blood  from  the  right 
ventricle  and  pulmonary  artery  passes  mainly  to  the  aorta  instead  of  to 
the  lungs.  To  carry  on  this  circulation,  the  wall  of  the  right  ventricle 
is  correspondingly  muscular  and  as  thick  as  that  of  the  left.  Toward 
the  end  of  fetal  life,  the  left  ventricle  becomes  thicker  and  heavier  than 
the  right. 

Weight  of  the  Adult  Heart  and  Position  of  the  Valves.  —  The  aver- 
age normal  adult  heart  weighs,  in  the  male,  from  280  to  360  grams 
(9i  to  12  oz.),  in  the  female,  from  240  to  330  grams  (8  to  11  oz.) ;  its 

proportion  to  body 
weight  ranges  approxi- 
mately from  1 :  160  to 
1 :  170.  Though  hearts 
vary  considerably  in 
size  within  normal 
limits,  the  average 
length  of  the  adult 
heart  on  its  longest 
axis  is  from  twelve  to 
fifteen  centimeters,  its 
greatest  breadth,  nine 
to  eleven  centimeters. 
The  adult  heart  lies 
behind  the  lower  two 
thirds  of  the  sternum. 
The  methods  for  deter- 
mining the  position  of 
the  valves  with  the 
heart  in  situ  by  frozen 
sections,  and  also  by  coating  the  valvular  surface  with  lead  and  subse- 
quently taking  radiographs,  have  not  given  uniform  results.  Accord- 
ing to  Piersol,  the  aortic  valves  lie  behind  the  left  half  of  the  sternum, 
a  little  below  and  to  the  right  of  the  pulmonary  valves ;  the  latter  are 
situated  behind  the  sternal  end  of  the  third  left  costal  cartilage. 
The  tricuspids  are  situated  behind  the  midsternum,  opposite  the  fourth 
interspace  and  the  fifth  chondro-sternal  articulation ;  the  mitral  valves 
are  opposite  the  sternal  end  of  the  third  left  interspace  (Fig.  2). 

Anatomy  and  Physiology  of  the  Heart.  —  The  heart  consists  of  three 
layers :  the  endocardium,  pericardium,  and  myocardium.  The  endo- 
cardium is  a  connective  tissue  membrane  containing  smooth  muscle 
and  numerous  elastic  fibers.  Its  free  endocardial  surface  consists  of  a 
single  layer  of  irregularly  shaped  polygonal  endothelial  cells.  The  epi- 
cardium  is  a  connective  tissue  structure  containing  fat  cells  and  elastic 
fibers;    its  outer  surface  is  covered  with  a  single  layer  of  squamous 


Fig.  2.  —  Diagrammatic  position  of  the  cardiac  valves. 
P.V  =  pulmonary  valves  ;         T.V  —  tricuspid  valves  ; 
A.V  =  aortic  valves  ;  M.V  =  mitral  valves. 


THE    HEART  3 

epithelium.  The  muscle  fibers  of  the  heart  although  transversely 
striated,  must  be  regarded,  developmentally  and  histologically,  as 
modifications  of  smooth  muscle.  The  undifferentiated  protoplasm  of 
the  heart  muscle  fiber  —  the  sarcoplasm  —  is  found  chiefly  in  its  axial 
part.  The  oval  nucleus,  which  frequently  contains  oil  droplets  or  pig- 
ment granules,  is  embedded  in  the  sarcoplasm.  The  muscle  cells  anas- 
tomose by  means  of  short,  oblique,  or  transverse  processes  into  various 
complexes  and  layers.  In  the  auricular  musculature  there  is  a  super- 
ficial muscular  layer  which  runs  transversely  and  encircles  both  auricles. 
Each  auricle  also  possesses  a  relatively  independent  system  of  fibers 
which  runs  at  right  angles  to  the  superficial  layers.  The  course  of  the 
ventricular  fibers  and  layers  is  quite  complex  and  as  yet  a  matter  of 
uncertainty.  According  to  the  most  reliable  studies,  the  fibers  on  the 
ventricular  surface  arise  from  tendinous  rings  and  membranes  at  the 
base  of  the  heart ;  here  they  form  a  vortex,  pass  into  the  interior  of  the 
left  ventricle  to  the  septum,  and  connect  with  the  papillary  muscles ; 
they  thus  turn  on  themselves  toward  the  base  and  form  spiral  loops,  which 
when  contracting,  approximate  base  and  apex,  and  at  the  same  time 
rotate  the  apex  clockwise  from  left  to  right.  Mall  divides  these  "  super- 
ficial fibers  "  into  two  groups :  the  Superficial  Bulbo-spiral  and  Super- 
ficial Sino-spiral.  The  former  belong  chiefly  to  the  left  ventricle.  They 
arise  from  the  conus  to  the  left  of  the  aorta  and  left  ostium  venosum, 
proceed  spirally,  penetrate  to  the  interior  of  the  left  ventricle  and  end 
in  the  septum  and  posterior  aspect  of  the  ventricle ;  at  that  point  they 
connect  with  the  posterior  papillary  muscles.  Some  of  the  deeper  fibers 
of  this  layer  encircle  the  lower  part  of  the  ventricle  and  pass  upward,  to 
end  at  the  base  of  the  heart.  The  superficial  sino-spiral  fibers  arise  mainly 
from  the  posterior  aspect  of  the  heart  in  the  neighborhood  of  the  right 
ostium  venosum,  proceed  spirally  (though  more  transversely  than  the 
first  group)  to  the  apex  over  the  anterior  surface  of  the  right  ventricle. 
They  penetrate  the  interior  of  the  left  ventricle  and  terminate  on  its 
anterior  surface  and  in  the  papillary  muscles,  especially  the  anterior. 
Beneath  the  superficial  layers  of  the  bulbo-  and  sino-spiral  systems  lie 
similar  deep  layers  which  run  more  transversely  or  circularly.  The 
deep  bulbo-spiral  layer  encircles  the  left  ventricle  and  ends  by  way  of 
the  septum  on  the  dorsal  side  of  the  aorta.  Some  fibers  make  a  circular 
loop  around  the  conus  at  the  base  of  the  pulmonary  artery.  The  entire 
layer  makes  a  strong  circular  system  whose  contraction  tends  to  diminish 
the  lumen  of  the  left  ventricle.  The  deep  sino-spiral  layer  originates 
from  the  posterior  aspect  of  the  left  ostium  venosum,  passes  transversely 
to  enter  the  interior  of  the  right  ventricle,  and  then  turns  upward  toward 
the  base.  Here  some  strands  pass  circularly  around  the  base  of  the  heart 
and  left  ostium. 

The  arterial  supply  of  the  heart  is  derived  from  the  right  and  left 
coronaries.  Though  often  so  regarded,  they  are  not  end  arteries,  for 
anastomoses  have  been  clearly  demonstrated  by  Spalteholz's  method. 


4  CLINICAL  CARDIOLOGY 

Furthermore,  blood  is  sometimes  found  beyond  an  old,  complete  obstruc- 
tion of  the  coronary  artery.  The  veins  accompany  the  arteries  and 
empty  in  the  right  auricle.  The  lymph  vessels  are  very  abundant; 
they  are  formed  from  radicals  derived  from  the  lymph  spaces  in  the 
clefts  between  the  muscle  fibers;  they  accompany  the  blood  vessels 
in  their  course  and  terminate  in  the  thoracic  and  right  lymphatic 
ducts. 

Attributes  of  the  Cardiac  Musculature.  —  Engelmann  and  Gaskell,  by 
careful  experimentation  some  thirty-five  years  ago,  established  certain 
attributes  of  the  cardiac  musculature,  namely :  irritability,  contractility, 
rhythmicity,  and  conductivity.  These  have  been  respectively  desig- 
nated by  Engelmann  as  bathmotropic,  inotropic,  chronotropic,  and  dromo- 
tropic  functions  ;  he  has  qualified  them  as  positive  or  negative,  depending 
upon  influences  which  act  favorably  or  unfavorably  upon  the  individual 
functions.  This  nomenclature,  however,  has  not  found  its  way  in 
general  clinical  use.  To  the  four  attributes  mentioned,  Gaskell  has 
added  a  fifth  —  tonicity.  This  property  is  similar  to  that  found  in 
ordinary  skeletal  musculature,  which,  in  the  case  of  the  heart,  keeps  it  in 
a  slight  state  of  contracture  even  during  diastole.  Tonicity  is  a  term 
which  is  perhaps  used  too  loosely  and  indiscriminately  and  is  often 
confused  with  the  contractile  power  of  the  heart;  it  is  the  attribute 
about  which  few  clinical  or  experimental  facts  are  known. 

It  is  necessary  to  emphasize  not  alone  the  differentiation  of  the 
various  cardiac  properties,  but  the  fact  that  certain  parts  of  the  heart 
are  endowed  with  these  properties  in  varying  degrees ;  for  example,  the 
sinus  region  with  rhythmic  attributes. 

Regarding  our  present  knowledge  of  these  various  functions,  it  may 
be  stated  that  though  much  is  known  about  disturbances  of  rhythm  and 
conductivity,  many  details  of  the  other  properties  are  still  wanting. 

Besides  the  cardiac  properties  mentioned,  another  is  that  each  systole 
is  of  maximum  intensity.  This  property  —  the  so-called  all-  or  none-re- 
action  —  means  that  the  heart  muscle  answers  any  stimulus  sufficient 
to  cause  response  by  a  maximal  contraction.  The  latter  is  probably  due 
to  the  intricate  intertwined  cardiac  muscular  system  already  described. 
Cardiac  contractility  therefore  does  not  depend  upon  the  strength  of  the 
impulse ;  it  varies,  however,  considerably  with  the  state  of  irrita- 
bility, one  of  the  heart  muscle  functions.  Regarding  this  function, 
during  systole  the  heart  is  not  irritable,  it  is  refractory  to  all  other  im- 
pulses and  therefore  cannot  be  tetanized  like  skeletal  musculature. 
There  is  an  experimental  exception  to  this  law ;  hearts  that  have  been 
poisoned  by  muscarine,  alcohol,  chloral,  etc.,  may  have  a  shortened 
refractory  phase  and  hence  may  be  brought  into  tetanic  contraction  by 
proper  stimuli. 

Nerve  Supply. — Situated  at  the  base  of  the  heart  are  the  intercom- 
municating superficial  and  deep  cardiac  plexuses,  from  which  the  ex- 
trinsic cardiac  nerves  are  derived.     The  superficial  plexus  lies  in  the 


THE  HEART  5 

concavity  of  the  aortal  arch ;  the  deep,  between  the  trachea  and  aorta. 
The  latter  plexus  is  composed  of  nerves  derived  from  the  sympathetic 
cervical  ganglia  and  the  cardiac  branches  of  the  recurrent  laryngeal 
and  vagus.  The  branches  from  the  right  side  of  the  plexus  go  to  form 
parts  of  the  anterior  and  posterior  coronary  plexuses,  besides  sending 
a  few  filaments  to  the  right  auricle.  The  branches  from  the  left  side 
are  distributed  to  the  left  auricle  and  compose  a  large  part  of  the  pos- 
terior coronary  plexus.  The  superficial  cardiac  plexus  forms  the  chief 
part  of  the  anterior  coronary  plexus. 

The  posterior  and  anterior  coronary  plexuses  surround  and  accom- 
pany the  branches  of  the  right  and  left  coronary  arteries,  respectively, 
and  distribute  filaments  to  the  ventricular  musculature.  The  coronary 
plexuses  as  well  as  their  muscular  filaments  are  richly  supplied  with 
ganglia. 

Intracardiac  ganglia  have  been  found  in  the  auricular  wall,  at  the 
entrance  of  the  superior  and  inferior  vena  cava  and  at  the  mouth  of  the 
coronary  sinus.  They  have  also  been  found  at  the  level  of  the  auriculo- 
ventricular  junction,  especially  about  the  aorta  and  the  pulmonary 
artery.  Scattered  ganglia  have  likewise  been  observed  in  the  upper  part 
of  the  ventricles.  One  observer  claims  to  have  discovered  ganglion 
cells  along  the  entire  ventricular  chamber. 

The  nerves  of  the  conduction  system  are  described  in  the  next 
chapter. 

The  extrinsic  nerves  to  the  heart  are  derived  from  the  cardiac  plexuses. 
The  heart  is  often  profoundly  influenced  by  impulses  which  reach  it 
from  these  nerves.  The  vagi  contain  the  inhibitory  fibers.  If,  in  the 
experimental  animal,  the  vagi  be  cut  in  the  neck,  the  cardiac  rate  is 
increased.  If  the  peripheral  ends  of  the  cut  vagi  be  stimulated,  there  is 
slowing  or  stoppage  of  the  heart,  or  a  condition  in  which  the  auricles  beat 
more  rapidly  than  the  ventricles  with  no  rhythmic  relationship  between 
the  two  (Complete  Heart  Block,  Chapter  VII).  In  warm-blooded 
animals  there  is  not  only  a  diminution  of  cardiac  rate,  but  also  of  the 
strength  of  auricular  and  ventricular  contraction,  until  the  heart  finally 
stops  in  diastole.  On  the  other  hand,  stimulation  of  the  cut  end  of  the 
sympathetic  produces  a  varying  degree  of  cardiac  acceleration.  De- 
pending upon  the  degree  of  stimulation  of  vagus  and  sympathetic,  the 
one  or  other  nerve  has  a  predominating  influence  upon  the  cardiac  rate. 
Though  antagonistic,  this  antagonism  cannot  be  measured  purely 
arithmetically ;  if  vagus  influence  predominates  during  the  course  of 
the  experiment,  after  cessation  of  stimulation,  a  typical  accelerator 
influence  results.  This  fact  in  itself  indicates  that  a  certain  amount  of 
tone  is  present  in  both  nerves.  Nerves  of  sensation  have  not  been 
discovered  in  the  heart.  Since  the  lower  cervical  and  upper  dorsal 
nerves,  which  supply  the  integument  of  the  neck,  chest,  and  upper  ex- 
tremity, also  send  filaments  to  the  deep  and  superficial  cardiac  plexuses, 
painful  skin  areas  of  varying  degrees  of  intensity  and  extent  are  found 


6  CLINICAL  CARDIOLOGY 

as  the  result  of  reflex  excitation  originating  in  the  heart  itself  from  some 
pathological  process  or  function  (Chapter  XXI). 

REFERENCES 

Chapter  I 

Einthoven,  W. :     Neuere  Ergebnisse  auf  dem  Gebiete  der  thierischen  Elek- 

tricitaet ;  Gesellsehaf  t  deutscher  Naturforscher  und  Aertzte ;  Verhandlung, 

1911. 
Engelmann,  T. :  Bijdrage  tot  de  Kermis  von  den  negatief-inotropen  invloed  .  .  . 

vagus  op  net  hart. 
Gaskell,  W.  H. :    On  the  Tonicity  of  the  Heart  and  Blood  Vessels ;    Journal  of 

Physiology,  1880,  III,  48. 
Gray's  Anatomy  ;  Edition  1901. 

His,  W. :   Beitraege  zur  Anatomie  des  menschliehen  Herzens. 
Howell's  Physiology,  5th  Edition. 

Lewis,  T. :  Pathology  of  the  Heart  Functions ;  Lancet,  October  10,  1914. 
Mackenzie,  J. :   Diseases  of  the  Heart,  3d  Edition. 
McCallum,  J.  B. :    On  the  Histogenesis  of  the  Striated  Muscle  Fibre  and  the 

Growth  of  the  Human  Sartorius  Muscle;  Johns  Hopkins'  Bulletin,  1898, 

IX,  208. 
Mall,  F.  P. :    Muscular  Architecture  of  the  Human  Heart ;    American  Journal 

of  Anatomy,  1910-1911,  XI,  211. 
Norris,  G.  H.,  and  Fetterolf,  G. :    The  Topography  of   the  Cardiac  Valves  as 

revealed  by  the  X-Ray ;  American  Journal  of  the  Medical  Sciences,  1913, 

CXLV,  225. 
Stohr,  P. :   Text  Book  of  Histology  ;   Edition  1901. 
Tigerstedt,  R. :    Lehrbuch  der  Physiologie  des  Menschens;  Edition  1911,  I. 


CHAPTER  II 


THE   CONDUCTION   SYSTEM 


N.f. 


Fig.     3.  —  Schematic     view    of    sino- 
auricular  node  of  dog,  showing  gen- 
eral form  of  the  node  and  differential 
structure.      A  =  artery  ; 
N.T  =  nodal  tissue  ; 
M.A  =  auricular  musculature. 


Position  and  Structure  of  the  Pacemaker.  —  Thorough  experimental 
electrocardiographic  investigations  in  mammals,  and  histological  and 
pathological  studies  in  man  and  ani- 
mals, have  proven  that  the  primum 
movens  —  the  normal  impulse  center 
in  the  human  being  — ■  exists  in  a  bit 
of  specialized  cardiac  tissue  situated  in 
the  sinus  region  immediately  beneath 
the  epicardium  and  in  the  groove  be- 
tween the  right  auricle  and  superior 
vena  cava.  This  rhythm  center  is 
variously  known  as  the  pacemaker, 
the  sino-auricular  node  (S-A  node), 
or  the  node  of  Keith-Flack.  Its  shape 
is  irregularly  pyriform  (Fig.  3)  with 

a  larger  upper,  and  a  somewhat  tapering  lower  end.     The  node  is 
surrounded  by  branches  of  the  vagus  and  sympathetic ;  it  contains  a 

plexus  of  moniliform  nerve  fibrils 
and  a  few  ganglionic  cells ;  it  is 
therefore,  histologically  considered,  a 
neuro-muscular  structure.  Its  blood 
supply  is  derived  from  a  special 
artery.  The  structure,  arrangement, 
and  composition  of  the  node  differ 
materially  from  the  remainder  of  the 
cardiac  musculature.  The  cells  are 
smaller,  stain  more  delicately,  and 
are  paler;  the  cross  striations  are 
indistinct  or  may  be  absent,  the 
nucleus  is  pale,  and  there  is  a  relative 
richness  of  perinuclear  sarcoplasm. 
The  cells  contain  more  glycogen  than 
those  of  the  non-specialized  muscle.  They  do  not  follow  any  orderly 
layer-like  arrangement,  but  are  placed  irregularly  in  a  rich  stroma  of 
fine  connective  tissue  (Fig.  4).     A  small  specialized  muscle  band  con- 

7 


NX... 


A.M. 


Fig.   4. — Detail  of   the  S-A   node  of 
dog  (high  power),  showing  the  cells. 
N.T  =  nodal  tissue  ; 
A.M.  =  auricular  musculature. 


8 


CLINICAL  CARDIOLOGY 


Fig.  5.  —  Right  ventricle  of  ox  heart,  showing  the  auriculo- 
ventricular  node  (A-V  node)  and  the  main  stem.  The 
right  branch  is  seen  running  along  the  "  Moderator  Band." 
(Modified  from  Tawara — "Das  Reitzleitungssystem  des 
Saugethierherzens. ") 


necting  the  sino-auricular  node  with  the  remainder  of  the  conduction 
system  has  been  described  by  Thorel,  but  its  presence  has  not  been 
corroborated  by  other  observers. 

Position  and  Distribution  of  the  Auxiculo-ventricular  Conduction 
System.  —  Similar  in  structure  to  the  sino-auricular  node  is  the  larger 

mass  of  specialized 
tissue,  known  as  the 
atrio-  or  auriculo- 
ventricular  conduc- 
tion system,  or  junc- 
tional tissue.  For 
purposes  of  anatomi- 
cal identification,  its 
various  parts  are  dif- 
ferently named,  but 
they  together  form 
one  continuous 
strand.  The  node 
of  Tawara  —  the  be- 
ginning of  the  junc- 
tional tissue  —  and 
the  bundle  of  His 
constitute  the  major 
part  of  the  conduction  system  before  its  division.  They  lie  imme- 
diately beneath  the  endocardium  in  the  lower  part  of  the  right  auricle, 
slightly  above  the  level  of  the  ventricle,  and  about  midway  between 
the  opening  of  the  coronary  sinus  and  the  fibrous  tissue  beneath  the 
aortal  cusps  (the 
aortic  vestibule  or 
"undefended 
space")-  The  con- 
duction system  is 
then  continued  into 
the  main  stem, 
which  soon  makes  a 
hairpin-like  division 
into  its  two  main 
branches  —  the 
right  (Fig.  5)  and 
left  (Fig.  6).  Both  FlG.6.. 
branches  course  on 
either  side  of  the  in- 
terventricular septum  in  a  direction  roughly  parallel  to  the  axes  of  the 
respective  ventricular  cavities,  and  are  contained  in  their  own  sheaths. 
The  right  branch  is  thin  and  spreads  out  in  a  somewhat  fan-shaped 
fashion;    the  left  is  more  compact,  thicker,  and  club-like.     In  their 


POST       A.CITTA1.     GUtf> 


RT.  ACUTA'-  CUSP 


■  Left  ventricle  of  ox  heart,  showing  conduction  sys- 
tem.    (Modified  from  Tawara.) 


THE   CONDUCTION  SYSTEM  9 

upper  portions,  both  branches  are  superficial  and  subendocardial.  They 
split  into  secondary  and  minor  branches  as  they  spread  toward  the  apex 
(Figs.  5,  6).  In  the  ox  heart,  the  left  branch  has  three  main  divisions  — 
to  the  anterior  and  posterior  papillary  muscles,  respectively,  and  to 
the  apex.  The  right  branch  has  one  division  that  goes  to  the  large 
papillary  muscle  and  venous  base,  the  other  forms  the  "  moderator  band  " 
which  supplies  the  septal  papillary  muscle  and  the  arterial  base  (conus 
arteriosis) ;  from  both  of  these,  a  division  to  the  apex  is  formed  from 
separate  heads.  The  branches  in  human  and  mammalian  hearts  finally 
divide  into  terminal  aborizations  (known  as  Purkinje  fibers  in  the  mam- 
mal) ,  which  ramify  through  the  papillary  muscles  and  probably  through- 
out the  entire  ventricular  musculature.  Some  of  these  terminal  aboriza- 
tions run  free  across  the  apical  portion  of  the  ventricular  cavities ;  they 
were  formerly  regarded  as  aberrant  tendinous  strands.  They  are 
macroscopically  distinguished  from  the  latter  by  their  paler  and  finer 
structure  and  non-glistening  appearance.  The  main  stem  and  branches 
of  the  conduction  system  are  sometimes  dimly  distinguished  through  the 
shimmering  endocardium  as  paler,  non-glistening  structures. 

Dissection  and  Demonstration  of  the  Conduction  System.  —  In 
order  to  dissect  out  the  conduction  system,  the  endocardium  over  the 
site  of  the  auriculo-ventricular  (A-V)  conduction  system  is  gently 
teased  off  with  forceps  after  the  heart  has  been  washed  in  water  and 
hardened  in  a  formaldehyde  solution.  The  conduction  system  is  most 
readily  dissected  in  the  ox  or  calf  heart,  less  readily  in  the  human. 
The  heart  is  first  incised  with  a  scalpel  near  the  margin  of  the  inter- 
ventricular septum.  The  ventricles  are  then  cut  parallel  to  the  latter. 
In  this  manner  they  can  be  turned  back,  and  the  septal  walls  of  the  auricle 
and  the  interventricular  septum  exposed  without  injury  to  the  con- 
duction system.  In  oxen  the  main  branch  on  the  right  side  exists  as 
a  separate  strand  —  the  moderator  band.  After  exposure  by  teasing 
in  the  manner  described,  the  structure  of  the  A-V  conduction  system  will 
be  found  paler,  softer,  and  more  delicate  than  that  of  the  surrounding 
musculature.  Another  method  of  gross  demonstration  of  the  conduction 
system  is  by  subendocardial  injection  of  the  main  branches  with  a  fine 
hypodermic  needle  and  syringe  containing  a  50  per  cent  solution  of 
India  ink.  If  carefully  performed,  not  only  the  main  branches  but  the 
subsidiary  divisions  stand  out  prominently  as  darker  strands.  In 
this  manner,  also,  corroborative  evidence  is  derived  that  ventricular 
contraction  begins  at  the  papillary  muscles,  for  the  ink  may  be  seen  to 
reach  the  latter  first  and  then  the  base  and  apex  of  the  heart. 

The  cellular  structure  of  the  main  junctional  tissue  is  similar  to  that 
of  the  S-A  node.  The  aborizations  consist  of  larger,  paler  cells  with 
large  nuclei  and  with  protoplasm  containing  faint  striations  at  the 
periphery. 

Arterial  and  Nerve  Supply  of  the  A-V  System.  —The  main  arterial 
supply  of  the  A-V  system  is  derived  from  a  special  branch  of  the  right 


10  CLINICAL  CARDIOLOGY 

coronary.  The  junctional  tissue  is  supplied  and  intertwined  with 
niedullated  nerve  fibrils  and  ganglia.  There  are  numerous  ganglion 
cells,  —  mono-,  bi-,  and  multipolar,  —  whose  processes  pass  to  adjacent 
ganglion  cells,  to  nerve  fibers  in  the  bundle,  or  through  the  A-V  system, 
some  of  which  end  in  ganglia  cells  of  the  bundle  or  in  the  muscle 
plexus.  There  is  an  intricate  plexus  of  varicose  fibrils  around  and  in 
close  relation  to  the  muscle  fibers  of  the  bundle.  Thus  the  A-V  system, 
like  the  sino-auricular  node,  is  a  neuro-muscular  spindle.  Though  the 
exact  distribution  to  the  nodes  of  the  extrinsic  cardiac  nerves  is  not 
known,  it  appears  probable  that,  regarding  the  vagus  distribution,  the 
S-A  node  is  supplied  chiefly  by  branches  of  the  right,  and  the  A-V 
by  those  of  the  left  vagus.  There  appears  to  be  a  similar  distribution 
to  the  S-A  and  A-V  nodes  by  the  right  and  left  accelerators,  respec- 
tively. 

Course  of  the  Normal  Impulse.  —  From  a  study  of  the  physiological 
and  anatomical  distribution  of  the  specialized  tissues,  it  is  evident  that 
the  normal  impulse  arises  in  the  S-A  node ;  it  spreads  thence  through  the 
auricle,  following,  as  far  as  known,  no  especially  differentiated  path  in  the 
latter.  It  then  reaches  the  junctional  tissue,  and  by  way  of  the  right 
and  left  branches  and  terminal  aborizations,  it  finally  spreads  to  the 
papillary  muscles  and  throughout  the  ventricular  musculature. 

Myogenic  or  Neurogenic  Impulse  ?  —  The  question  whether  the 
original  impulse  is  of  myogenic  or  neurogenic  origin  has  been  for  years 
a  matter  of  dispute,  and  has  not  yet  been  decided.  The  intimate  and 
intricate  relationship  existing  between  the  muscle  and  nerve  structures 
in  the  nodal  regions  demonstrates  how  difficult  must  be  the  final  deter- 
mination of  this  question.  It  is  known  clinically  that  the  rhythm  center 
is  readily  influenced  by  purely  neurogenic  impulses ;  these  can  indeed 
upset  the  normal  cardiac  control  and  give  rise  to  abnormal  rhythms 
(Chapter  VIII).  How  far  such  clinical  observations  can  be  applied  to 
the  question  of  the  normal  control  of  the  rhythm  center  it  is  impos- 
sible to  state.  All  in  all,  it  seems  probable  that  the  sino-auricular  node  is 
activated  by  both  neurogenic  and  myogenic  influences,  though  we  have 
at  present  no  means  of  discovering  under  what  circumstances  either 
becomes  the  controlling  factor. 


REFERENCES 
Chaptek  II 

Aschoff,  L. :  Referate  ueber  die  Herzstoerungen  der  specifischen  Muskelsystems 

des  Herzens ;    Verhandlungen  der   deutschen  pathologischen  Gesellschaf t, 

1910. 
Cohn,  A.  E. :    Observations  on  Injection  Specimens  of  the  Conduction  System 

in  Ox  Hearts ;  Heart,  1912-1913,  IV,  225. 
Cohn,  A.  E.,   Kessel,  L.,  and  Mason,  H.  H. :  Observations  on  the  Functions  of 

the  Sino-auricular  Node  in  the  Dog;  Heart,  1911-1912,  III,  311. 


THE   CONDUCTION   SYSTEM  11 

Cohn,  A.  E.,  and  Lewis,  T. :  The  Predominant  Influence  of  the  Left  Vagus  on 
Conduction  between  Auricle  and  Ventricle  in  the  Dog ;  Journal  of  Ex- 
perimental Medicine,  1913,  XVIII,  739. 

Engel,  I. :  Beitraege  zur  normalen  und  pathologischen  Histologic  des  atrio- 
ventrikularen  Buendels ;   Ziegler's  Beitrage  zur  pathologischen  Anatomie, 

1910,  XLVIII,  499. 

Keith,  A.,  and  Flack,  M. :  The  Form  and  Nature  of  the  Muscular  Connections 
between  the  Primary  Divisions  of  the  Vertebrate  Heart ;  Journal  of  Anat- 
omy and  Physiology,  1907,  XLI,  172. 

Lewis,  T. :   Lectures  on  the  Heart. 

Lewis,  T.,  Oppenheimer,  B.  S.,  and  Oppenheimer,  A. :  The  Site  of  Origin  of 
the  Mammalian  Heart  Beat ;   The  Pacemaker  in  the  Dog ;    Heart,   1910- 

1911,  II,  147. 

Lhamon,  R.  M. :  The  Sheath  of  the  Sino- ventricular  Bundle  ;  American  Journal 

of  Anatomy,  1912,  XIII,  55. 
Oppenheimer,  B.  S. :   A  Routine  Method  of  Opening  the  Heart  with  Conserva- 
tion of  the  Bundle  of  His  and  the  Sino-aurieular  Node  ;  Journal  of  American 

Medical  Association,  1912,  LIX,  937. 
Oppenheimer,  B.  S.,  and  Oppenheimer,  A. :   Nerve  Fibrils  in  the  Sino-aurieular 

Node;  Journal  of  Experimental  Medicine,  1912,  XVI,  613. 
Tawara,  S. :  Das  Reitzleitungssystem  des  Saeugethierherzens. 
Thorel,  C. :    Vorlaeufige  Mittheilung  ueber  eine  besondere  Muskelverbindung 

zwischen  der  Cava  Superior  und  dem  Hissischen  Buendel ;    Muenchener 

Med.  Wochenschrift,  1909,  LVI,  2159. 
Wilson,  J.  G. :  The  Nerves  of  the  Atrio-ventricular  Bundle  ;  Proceedings  of  the 

Royal  Society,  1909,  B,  LXXXI,  151. 


CHAPTER  III 

POLYGRAPHIC   TRACINGS 

Mackenzie  Ink  Polygraph.  —  For  purposes  of  exact  study  of  arterial 
and  venous  pulsations,  mechanical  methods,  instruments,  and  graphic 
representation  (sphygmograms)  are  necessary. 

Instruments  that  simultaneously  transcribe  arterial  and  jugular 
pulsations  are  called  polygraphs.  For  clinical  use  I  have  found  the 
Mackenzie  Ink  Polygraph  perfectly  satisfactory.  Its  compact  size, 
the  comparative  simplicity  and  ease  of  operation,  the  fact  that  if  neces- 
sary very  long  records  can  be  taken,  and  the  use  of  ink  and  a  paper  roll 
instead  of  smoked  paper,  make  it  suitable  for  clinical  work. 

The  Mackenzie  polygraph  (Fig.  7,  Plate  I)  consists  essentially  of  a 
clockwork  (CI)  incased  in  a  metal  container.  The  clock  is  fitted  with  a 
time-marker  ( Ti)  which  ticks  and  marks  fifth  seconds  by  means  of  a  small 
pen.  The  speed  of  the  time-marker  may  be  regulated  by  a  small  screw  (S) . 
There  are  two  separate  keys  (S.B  1,  S.B  2)  for  winding  the  driving  gear 
and  the  time-marker.  There  is  also  a  small  lever  (Le)  which  starts  and 
stops  the  driving  mechanism.  Attached  to  one  side  of  the  case  is  a 
slot  (ST)  into  which  is  fitted  a  support  for  a  paper  roll  (Pr).  On  the 
opposite  side  is  a  smaller  slot,  which  acts  as  a  rest  for  a  long,  narrow  arm 
(Ar)  for  the  support  of  two  transmitting  tambours  (T.T) ;  the  latter 
are  so  arranged  that  they  can  move  in  any  direction.  To  the  tambours 
are  attached  long  writing  pens  (P) ;  the  pressure  of  the  points  upon 
the  paper  may  be  regulated  by  manipulating  the  tambours.  Each 
tambour  is  also  separately  connected  with  the  receiving  apparatus 
applied  to  the  venous  and  arterial  pulse  by  means  of  elastic  tubing  (E.  T). 
The  receiver  for  the  venous  pulsations  is  a  small  circular  metal  cup 
(Cu),  which  may  also  be  used  for  registering  cardiac  pulsations  by  plac- 
ing it  over  the  apex.  For  transmitting  radial  pulsations,  a  perforated 
leather  strap  (L.S)  is  buckled  about  the  wrist  and  so  adjusted  that  the 
button  (Bit)  or  pelotte  rests  upon  the  most  prominently  pulsating  part 
of  the  radial ;  the  pressure  of  the  pelotte  upon  the  latter  is  regulated 
by  a  small  flat  spring  (Sp).  There  is  a  broad  wrist  tambour  (W.T) 
which  rests  upon  the  button  and  transmits  radial  pulsations  to  the 
writing  pens  through  the  transmitting  tambour. 

12 


PLATE   I 


Fig.  7.  —  Mackenzie  Ink  Polygraph. 

CI  =  Clockwork ; 
Ti  =  Time-marker ; 

aS  =  Screw  which  regulates  speed  of  time-marker; 
S.B  1,2=  Keys  for  winding  the  driving  gear  and  time-marker; 

Le  =  Lever  for  starting  and  stopping  the  driving  mechanism  ; 
SI  =  Slot  for  support  of  the  paper  roll  (P.R) ; 

At  =  Arm  for  the  support  of  the  two  transmitting  tambours  (T.T)  ; 
P  =  Writing  pens  ; 
E.T  =  Elastic  tubing  connecting  the  transmitting  tambours  to  the  receiving  apparatus ; 
Cu  =  Cup  for  receiving  venous  or  cardiac  pulsations ; 
L.S  =  Leather  strap  for  buckling  over  the  radial  artery ; 
Bu  =  Button  for  receiving  the  radial  pulsations ; 

Sp  =  Screw  for  regulating  the  pressure  of  the  button  upon  the  radial ; 
W.T  =  Wrist  tambour. 


POLYGRAPHIC  TRACINGS 


13 


Poi-yeRAPti  RcceiVen- 


Method  of  Use  of  the  Mackenzie  Polygraph.  —  The  polygraph  is 
used  as  follows :  the  driving  mechanism  and  time-marker  are  wound 
up,  the  paper  roll  set  in  place,  the  pens  thoroughly  inked  and  lightly 
adjusted  upon  the  paper.  After  palpating  the  radial,  its  most  pul- 
satile point  is  marked  by  an  ink  spot,  or  preferably  by  two  rectangular 
lines  (  |~)>  one  along  the  radial,  the  other  across  the  wrist;  these  serve 
as  guides  for  the  proper  position  of  the  pelotte  and  wrist  strap.  The 
best  position  of  the  wrist  is  with  the  hand  in  moderate  extension  or 
hyperextension,  because  this  tends  to  make  the  radial  artery  more  super- 
ficial. This  position  can  be  conveniently  maintained  by  firmly  pressing 
the  extended  hand  against  the  physician's  thigh.  The  upper  strap  of 
the  wrist  attachment  is  put  on  loosely  so  as  not  to  obliterate  the  artery ; 
the  lower  is  buckled  on  firmly.  The  spring  regulating  the  pressure 
of  the  pelotte  is  then  pressed  down  sufficiently  to  make  the  latter  bob 
vigorously  with  the  radial  pulsations.  The  wrist  tambour  is  slipped  in 
position  with  its  screw  sup- 
port loose,  so  that  the  ^—^  c 
metal  tip  on  the  under  sur- 
face of  the  tambour  rests 
full  upon  the  bobbing  but- 
ton; it  is  then  screwed 
and  held  in  this  position. 
Thus  through  the  receiv- 
ing and  transmitting  air 
system  of  tambours  and 
their  connecting  elastic 
tubing,  the  radial  pulsa- 
tions are  transmitted  to 
the  writing  pens. 

To  transmit  and  tran- 
scribe   venous    pulsations 

the  metal  cup  is  placed  over  the  jugular  bulb  (Fig.  8),  preferably  on 
the  right  side,  because  the  vein  is  usually  more  prominent  on  that 
side.  The  neck  of  the  cup  is  grasped  between  the  fore  and  middle 
fingers,  the  rim  by  the  thumb,  and  the  cup  slid  along  the  outer  border 
of  the  sterno-mastoid  muscle  until  it  touches  the  clavicle.  It  thus 
rests  over  the  triangular  area  formed  by  the  jugular  vein  (with  its 
bulb),  the  inner  end  of  the  clavicle,  and  the  sterno-mastoid  muscle. 
The  patient  is  made  to  lie  as  flat  as  possible ;  he  should  breathe 
quietly,  for  stertorous  breathing  interferes  with  proper  registration. 
Rigidity  of  the  neck  muscles  also  mars  pulsations.  Superabundance  of 
fat  and  respiratory  dyspnoea  are  other  factors  which  may  interfere 
with  or  vitiate  accurate  registration. 

After  the  wrist  tambour  and  venous  cup  have  been  satisfactorily 
adjusted,  the  pens  are  separately  slid  across  the  paper,  so  as  to  establish 
coincident  ordinates  for  measurement  of  the  curves.     These  lines  need 


Fig.  8.  —  Schematic  view  of  the  a-c-v  waves  and  of 
the  jugular  bulb. 


14 


CLINICAL  CARDIOLOGY 


not  necessarily  be  continuous,  for  simultaneous  venous  and  arterial 
pulsations  may  be  measured  off  and  standardized  by  means  of  calipers. 
The  driving  mechanism  is  now  released  and  arterial  and  venous  pulsa- 
tions simultaneously  registered. 

Correlation  between  Experimental  Auricular  Pressure  Curves  and 
the  Human  Jugular  Pulse.  —  Early  experimenters  gained  information 
regarding  auricular  pressure  curves  by  inserting  sounds  directly  into  the 
auricles  of  dogs  and  horses  ;  they  found  that  auricular  contractions  were 
accompanied  by  increased  auricular  pressure,  that  is,  by  positive  pres- 
sure waves.  While  there  is  a  general  correspondence  between  such 
pressure  curves  and  human  jugular  tracings  obtained  by  the  polygraph, 
it  must  be  remembered  that  the  latter  primarily  depend  upon  difference 
in  volume  created  in  the  confined  air  space  of  the  cup  resting  over  the 
jugular  bulb.  These  volumetric  differences  are  transmitted  to  the 
tambour,  and  the  pen  is  then  correspondingly  deflected.  Hence  dif- 
ferences in  auricular  pressure  are  not  necessarily  transmitted  and  tran- 
scribed as  volumetric  waves ;  and  as  a  corollary,  one  can  rarely  predicate 
and  estimate  auricular  pressure  by  the  excursion  and  direction  of  the 
"  venous  "  poly  graphic  waves. 

The  Waves  of  the  Normal  Jugular  Pulse,  —  the  Normal  Phlebo- 

gram.  —  Frequent  observations  have  shown  that,  corresponding  to  the 

j_„  first  auricular  pressure  curve 

coincident  with  auricular 
systole,  there  exists  normally 
a  venous  pulse  best  seen  in 
the  venous  trunks  at  the  root 
of  the  neck.  In  man,  for 
each  radial  beat,  there  are  in 
the  normal  jugular  tracing 
three  waves  or  elevations; 
each  elevation  is  accompanied 
by  a  corresponding  depres- 
sion (Fig.  9).  We  shall  fol- 
low the  simple  nomenclature 
usually  adopted  in  the  litera- 
ture and  call  the  elevations  the  a-c-v  waves.  The  a  refers  to  the 
auricular,  c  to  the  carotid,  and  v  to  the  ventricular  filling  wave.  The 
rise  (Figs.  8-9)  and  fall  (Figs.  8-9,  1)  of  the  first  wave  a  are  caused  by 
the  reflux  wave  produced  in  the  veins  of  the  neck  by  auricular 
systole.  In  rhythmically  beating  hearts,  the  a  wave  comes  before 
the  advent  of  ventricular  systole  (c  wave).  The  absence  of  the  a 
elevation  in  those  types  of  arrhythmia  in  which  experimental  and 
electrocardiographic  evidence  shows  absence  of  normal  rhythmic  au- 
ricular contractions  (Auricular  Fibrillation,  Chapter  VII),  and  its 
abnormal  position  in  arrhythmias  affecting  relationship  between  auricu- 
lar and  ventricular  contractions  (Heart  Block,  Chapter  VII),  are  con- 


30CUi.AR 


Fig.  9.  —  Diagrammatic  representation  of  the  nor- 
mal polygraphic  curve. 
a  —  auricular  wave  ; 
c  =  carotid  wave  ; 
v  =  ventricular  filling  wave.     (See  text.) 


POLYGRAPHIC   TRACINGS 


15 


firmatory  evidence  that  the  a  wave  is  in  the  main,  if  not  entirety, 
due  to  auricular  systole.  If  the  jugular  tracings  were  quite  similar  to 
the  experimental  auricular  pressure  curves,  following  auricular  systole 
(a  wave)  there  should  be  a  continuous  fall  (Fig.  9,  1-2)  and  two  eleva- 
tions (a-v)  and  depressions  (2-3)  in  the  venous  tracing.  The  post- 
auricular  fall  is  interrupted  by  the  advent  of  an  elevation,  the  c  wave. 
For  the  present  disregarding  the  latter,  the  chief  cause  of  the  postauric- 
ular  fall  of  pressure  (Figs.  8-9, 1-2)  is  undoubtedly  auricular  relaxation 
following  systole ;  ventricular  systole  acts  as  a  contributory  cause  in 
increasing  this  relaxation,  mainly  by  dragging  down  the  interventricular 
septum,  and  to  a  lesser  degree,  by  producing  diminished  intrathoracic 
pressure.  The  physiological  limit  of  the  duration  of  the  a  wave  is 
one  fifth  of  a  second. 

The  cause  of  the  carotid  wave  is  still  a  matter  of  dispute.  Its  oc- 
casional appearance  one  twentieth  of  a  second  before  the  onset  of  ca- 
rotid pulsation,  and  its  presence  after  experimental  ligation  have  been 
offered  as  evidence  that  the  c  wave  is  not  due  to  carotid  pulsation.  How- 
ever, those  who  have  worked  with  the  cup  receiver  over  the  jugular  bulb 
will  have  observed  how  the  venous  tracing  is  often  vitiated  by  placing  the 
receiver  too  close  to  the  carotid,  in  consequence  of  which  the  c  wave  will 
often  obtrude  itself  upon  the  venous  tracing.  Although  there  exists  some 
dispute  as  to  its  cause,  the  practical  importance  of  the  incidence  of  the 
c  wave  in  the  study  of  the 

"*/§P* — »— 


W        V       »■•«•• 


^hymAJ 


human  phlebogram  rests 
upon  the  fact  that  its  foot 
point  is  coincident  with  the 
onset  of  carotid  pulsation. 
The  determination  of  the 
foot  point,  therefore,  be- 
comes an  important  land- 
mark in  the  study  of  the 
polygram.  Since  the  pulse 
wave  reaches  the  wrist  ap- 
proximately one  tenth  of  a 
second  after  its  arrival  at  the 
carotid  artery,  and  the  onset 
of  the  individual  radial  beats  is  readily  discernible  in  the  arteriogram, 
the  foot  point  of  the  c  wave  may  be  determined  and  distinguished 
from  the  a  and  v  waves  by  measuring  with  calipers  from  coincident 
ordinates  in  the  radial  and  venous  tracings.  These  ordinates  are 
derived  by  stopping  the  driving  mechanism  for  a  moment  and  sliding 
both  pens  across  the  paper  (Fig.  10) ;  when  measuring  in  the  direction 
of  the  physiological  progression  of  the  waves,  one  tenth  of  a  second 
(the  difference  in  time  between  carotid  and  radial  pulsations)  is  added  ; 
in  this  manner  the  foot  point  of  the  c  wave  is  derived.  With  the  latter 
determined,  it  becomes  a  simple  matter  in  good  curves  to  determine  the 


Fig.  10.  —  Normal  venous  and  radial  tracing  show- 
ing rhythmical  a-c-v  waves  in  the  jugular  trac- 
ing, and  regular  radial  beats.  The  points  S-S  are 
coincident  ordinates  derived  by  sliding  the  pens 
when  the  driving  mechanism  is  at  rest.  The 
method  of  derivation  of  the  foot  point  of  the 
c  wave  is  also  shown. 


16 


CLINICAL  CARDIOLOGY 


a  and  v  waves  when  the  pulse  beats  rhythmically :  the  precarotid  is 
the  a,  and  the  postcarotid,  the  v  wave. 

The  third  positive  (Fig.  9,  v),  the  ventricular  wave  which  follows 
the  second  depression,  is  due  to  ventricular  systole ;  it  results  almost 
entirely  from  reflux  of  the  stored  auricular  blood  which  is  forced  into 
the  venous  system  with  ventricular  systole  while  the  auriculo-ventricular 
valves  are  still  closed.  Another  factor  in  its  production  is  the  sudden 
release  of  the  base  of  the  ventricle  at  the  commencement  of  ventricu- 
lar diastole.  The  slightly  variable  beginning  of  the  v  wave  depends 
upon  the  varying  amount  of  blood  stored  up  during  auricular  diastole ; 
its  termination  is  coincident  with  the  opening  of  the  tricuspid  valves. 

The  third  fall  or  depression  (Fig.  9,  3)  is  caused  by  the  rapid  drop 
of  pressure  in  the  auricle  and  in  the  venous  trunks  at  the  root  of  the  neck, 
which  follows  the  beginning  of  ventricular  diastole  and  the  opening  of 
the  auriculo-ventricular  valves. 


Translating  the  knowledge  gained  from  the  graphic  orderly  sequence 
of  auricular  and  carotid  pulsations  (the  a  and  c  waves)  into  terms  of 
auricular  and  ventricular  systoles,  we  have  the  means  of  studying 
rhythmical  sequential  cardiac  cycles  —  the  normal  pulse  —  as  well 
as  the  numerous  disturbances  of  rhythm  affecting  auricle  and  ventricle. 

Variations  in  the  Normal  Phlebogram.  —  There  are  certain  varia- 
tions in  the  normal  phlebogram  which  require  consideration.     The  a 


»  p   w   *Tte*    W 


*  •  0 


■     »  r    <?     <r    <f     «7/9- 


w 

e  y  c 


~~**~ 


ww* 


-iftjtr      -^Kastf— 


Figs.  11,  12,  13.  —  These  figures  show  a  split  c(c-c)  wave  in  the  venous  tracing. 

wave  is  occasionally  bifurcated  at  its  apex,  i.e.  at  the  height  of  auricular 
systole ;  such  splits  I  believe  result  from  a  venous  reflux  wave  produced 
u...y-.,..  «■-..-  by  a  sharp  flapping  action  of  the  valves 
J^^Z^XX^yZ^    in  the  jugular  bulb. 

The  c  wave  is  sometimes  split  (Figs. 
11,  12,  13).  When  this  occurs,  the  first 
part  is  usually  high  and  its  fall  sharp. 
It  is  due  to  the  fling  of  the  lever  caused 
by  placing  the  cup  too  close  to  the  ca- 
rotid, or  to  causes  similar  to  those  of  the 
dicrotic  notch  of  the  radial  (q.v.).  An- 
other variation  of  the  phlebogram  is  the 
occasional  blending  of  venous  and  arterial  tracings ;  the  c-v  waves  then 


Fig.    14.  —  Combined    venous    and 
arterial  tracing  in  the  jugular. 


POLYGRAPHIC  TRACINGS 


17 


resemble  an  arteriogram  (Fig.  14).  The  v  wave  is  sometimes  divided; 
this  division  is  probably  caused  by  the  two  factors  in  its  production 
(q.v.)  acting  somewhat  asynchronously. 

Another  wave  —  the  so-called  h  wave  —  is  sometimes  seen  in  mid- 
diastole  or  directly  preceding  the  a  peak  (Figs.  15,  16).  It  is  regarded 
as  due  to  the  rather  sharp  balloon- 
ing of  the  tricuspids  by  the  rush  of 
inpouring  blood  during  diastole. 

Limitation  of  Inferences  from  the 
Phlebogram.  —  With  reference  to  in- 
formation derived  from  the  normal 
rhythmic  tracing,  it  must  be 
phasized  that,  be- 
cause of  the  me- 
chanical limitations 
of  the  polygraph, 
because  the  waves 
measure  volumetric 
changes,  and  be- 
cause of  the  manner 
of  application  of  the  venous  cup,  only  very  rarely  can  conclusions  re- 
garding auricular  or  ventricular  energy  be  drawn.  I  have,  for  example, 
taken  many  venous  tracings  from  patients  with  valvular  and  myo- 

Figs.  17-24.  —  Jugular  tracings  of  patients  with  heart  disease,  showing  variations  in  the 
heights  of  the  waves.  The  variations  are  not  distinctive  of  any  type  of  valvular 
disease. 


Figs.  15,  16.  —  These  show  an  h  wave. 


Fig.  17.  —  Normal 
phlebogram  from  a 
case  of  aortic  regur- 
gitation. 


Fig.  18. —  R  =  radial  trac- 
ing. Normal  jugular 
tracing  from  a  patient 
with  aortic  stenosis  and 
a  double  mitral  lesion. 


Fig.  19.  —  Normal  jugular  trac- 
ing from  a  patient  with  aortic 
stenosis  and  a  double  mitral 
lesion. 


m  t,t  »»«»»»»>     »»     »     ■     t    t* 


Fig.  20.  —  Normal  sized  a  and  other 
peaks  from  a  case  of  mitral  stenosis. 


Fig.    21.  —  Normal   a  wave   from   a 
case  of  mitral  regurgitation. 


18 


CLINICAL   CARDIOLOGY 


cardial  lesions,  and  after  comparison  with  normal  tracings,  I  have  been 
unable  to  discover  any  distinction  between  them.  Figures  17-24  taken 
from  patients  with  various  diseases  illustrate  this  fact. 


Figs.  22,  23,  24.  —  Normal  jugular  tracing  from  cases  of  exophthalmic  goiter. 

The  Radial  Pulse.  —  Because  of  the  method  of  instrumental  ap- 
plication —  a  spring  and  pelotte  pressing  upon  the  radial  artery  —  the 
arterial  sphygmogram  represents  differences  of  arterial  pressure.  The 
amount  of  spring  tension  required  to  sufficiently  occlude  the  artery  for 
the  purposes  of  tracing  is  quite  variable,  hence  the  resultant  curve  is 
in  many  instances  no  accurate  or  even  approximate  measure  of  the 
amount  of  arterial  pressure.  In  addition  to  these  mechanical  draw- 
backs, extraneous  factors,  e.g.  the  position  of  the  radial,  its  accessi- 
bility, the  pliability  of  its  walls,  etc.,  are  considerations  which  profoundly 
modify  inferences  drawn  from  the  pulse  tracing.  The  special  value 
derived  from  the  radial  tracing  in  the  polygram  rests  upon  knowledge 
gained  regarding  cardiac  rate  and  rhythm,  and  the  aid  in  fixing  the 
time  relation  of  events  in  the  cardiac  cycle ;  the  foot  point  of  the  radial 
serves  as  a  standard  for  determining  the  incidence  of  the  c  wave  in  the 
venous  tracing. 

The  first  wave  of  the  radial  (Figs.  25,  26,  1-2),  usually  called  the 
primary  or  percussion  wave,  is  generally  steep,  its  fall  sharp.     It  is  due 


Figs.  25,  2G.  —  Normal  radial  pulse  tracings. 

1-2  =  abrupt  rise  probably  due  to  instrumental  fling  of  the  lever  (also  called  primary 
or  percussion  wave)  ; 

1-3  =  time  of  ventricular  systole  —  the  aortic  valves  are  open  ; 
D.N  =  dicrotic  notch  ; 
D.W  =  dicrotic  wave  ; 
S.W  =  systolic  wave  (also  called  tidal  and  predicrotic  wave). 


to  the  sudden  instrumental  fling  given  to  the  pelotte  and  lever  by  the 
sharp  impact  of  the  onrushing  blood.     It  occurs  in,  and  is  part  of,  the 


POLYGRAPHIC   TRACINGS  19 

wave  produced  by  systolic  arterial  distention,  and  may  be  regarded  as 
an  initial  artificial  peak  superimposed  upon  the  arterial  wave  during 
systole.  It  is  immediately  followed  by  the  systolic  wave,  sometimes 
called  the  secondary  tidal  or  predicrotic  wave  (Figs.  25,  26,  SAY,  2-3). 
The  termination  of  the  systolic  and  the  beginning  of  the  dicrotic  wave 
(Figs.  25,  26,  DAY)  is  marked  by  the  dicrotic  notch  (Fig.  25,  D.N). 
This  notch  corresponds  to  certain  events  in  the  cardiac  cycle :  the  end 
of  the  ventricular  systole  and  the  foot  point  of  the  v  wave  in  the  venous 
tracing  (Fig.  26).  Other  small  waves  are  sometimes  found  in  the  radial 
tracing ;  their  cause  and  significance  are  not  known. 

The  cause  of  the  dicrotic  wave  is  still  in  dispute.  Mackenzie  re- 
gards it  as  due  to  sudden  relaxation  of  the  ventricular  wall,  including 
that  portion  supporting  the  aorta :  according  to  him  there  is  thus  de- 
veloped a  tendency  to  the  production  of  a  negative  aortic  wave,  which 
is  checked  by  the  sudden  stretching  of  the  membranous  aortic  valves, 
thereby  causing  a  second  positive,  the  dicrotic  wave.  It  has  been 
experimentally  demonstrated  in  a  circulatory  model  in  which  the  arterial 
system  is  represented  by  elastic  tubing,  that  sudden  check  of  the  inflow 
produces  a  suction  or  negative  pressure  behind  the  column  of  fluid, 
and  with  it,  resultant  waves.  Indeed,  "  dicrotic  "  waves  have  been 
produced  in  an  "  arterial  system  "  in  which  the  pumping  mechanism  was 
a  syringe  not  comparable  to  the  heart,  a  fact  showing  that  these  waves 
may  be  entirely  the  result  of  pressure  effects  in  elastic  arteries.  With 
the  influx  of  fluid,  the  tube  expands ;  with  the  sudden  cessation  of 
the  flow,  the  resultant  negative  pressure  in  a  rigid  tube  would  lead 
only  to  a  reflux  of  fluid.  In  elastic  tubing,  however,  represented  in  the 
human  being  by  the  aorta,  there  is  the  additional  force  of  elastic  recoil. 
Both  forces  —  suction  and  elastic  recoil  —  produce  shrinkage  be- 
yond the  natural  caliber  of  the  tube  (aorta),  the  elastic  constricted 
caliber  causing  secondary  expansion  and  with  it  the  secondary  pul- 
satile "  dicrotic  "  wave.  Similar  physical  facts  present  in  the  arterial 
system  seem  to  me  sufficient  to  cause  dicrotic  waves.  It  is  known, 
for  example,  that  when  the  ventricles  relax,  the  pressure  in  those 
chambers  falls  rapidly  and  the  semilunar  valves  close ;  there  is  in 
consequence  a  negative  pressure  at  the  mouth  of  the  aorta,  "  accom- 
panied by  an  actual  though  slight  movement  of  the  blood  current " 
(Wiggers).  The  element  of  elasticity  in  the  human  aorta  has  already 
been  mentioned. 

It  has  also  been  held  that  the  dicrotic  wave  is  reflected  from  the 
periphery.  Under  such  circumstances,  the  distance  between  dicrotic 
and  primary  crests  ought  to  diminish  as  the  arteries  recede  in  distance 
from  the  heart,  and  there  should  be  no  dicrotism  in  the  proximal 
part  of  the  compressed  artery.  Both  of  these  suppositions  are  dis- 
proved by  sphygmographic  tracings.  In  addition  the  manifold  ar- 
terial division  at  the  periphery  would  seem  to  make  one  large  reflected 
wave  impossible. 


20  CLINICAL   CARDIOLOGY 

The  height  of  the  dicrotic  notch  is  ordinarily  about  one  half  of  the 
arterial  curve.  In  some  cases,  with  sharp  fall  of  arterial  pressure  fol- 
lowing ventricular  systole,  the  notch  is  abnormally  low.  This  happens 
frequently  in  aortic  regurgitation  with  cardiac  failure  (Fig.  27),  but  it 


Mml 


Fig.    27.  —  Low    dicrotic    notch    (d)  Fig.  28.  —  Low  dicrotic  notch  (d)  from  a  case 

from  a  case  of  aortic  regurgitation  of  aortic  aneurism  with  cardiac  failure, 

with  decompensation. 

is  also  found  in  other  decompensated  heart  lesions,  valvular  or  myo- 
cardial in  origin  (Fig.  28). 

Types  of  Pulse.  —  From  what  has  preceded,  it  is  evident  that  only 
exceptionally  can  definite  conclusions  regarding  the  "  strength  "  or 
"  weakness  "  of  the  circulation  be  drawn  from  graphic  records.  In  fact, 
the  terms  "  weak  "  and  "  strong  "  pulse  are  usually  misapplied  to  what 
should  properly  be  called  "  soft  "  and  "  hard,"  respectively.  The  old 
terms  previously  in  use  have  the  advantage  of  describing  the  physical 
impression  given  to  the  examining  finger.  When  thus  descriptively 
applied  and  no  deductions  regarding  the  state  of  circulation  are  drawn, 
they  serve  a  useful  purpose.  These  terms  and  their  definitions  are  as 
follows :  a  sudden  fall  of  the  pulse  wave  produces  what  is  known  as  the 
"  collapsing  "  pulse ;  if  extreme,  it  becomes  the  typical  "  water  hammer  " 
or  Corrigan  pulse.  The  radial  pulse  can  also  be  described  as  large  and 
expansile  (pulsus  magnus),  small  or  compressible  (p.  mollis),  or  hard 
and  incompressible  (p.  durus).  The  rise  of  the  pulse  wave  may  be  quick 
(p.  celer)  or  slow  (p.  tardus).  If  dicrotism  becomes  palpable,  the  pulse 
is  known  as  dicrotic ;  if  the  dicrotic  notch  breaks  low  and  the  dicrotic 
wave  is  marked,  it  is  called  hyperdicrotic.  Occasionally,  the  pulse 
wave  feels  unduly  sustained  at  the  point  of  its  maximal  pulsation  and 
falls  slowly, — the  anacrotic  pulse.  The  bisferiens  gives  the  sensation 
of  a  double  pulsatile  impact;  it  is  produced  by  the  rather  equal  split 
of  the  systolic  plateau  by  the  predicrotic  or  instrumental  wave.  Its 
assumed  significance  as  evidence  of  aortic  stenosis  is  not  borne  out  by 
clinical  experience. 

Important  information  of  the  state  of  the  radial  artery  is  sometimes 
gained  by  careful  palpation.  Marked  nodosity,  thickening,  and  tor- 
tuosity are  immediately  apparent.  The  opposite  information  —  that 
of  a  normal  elastic  arterial  wall  —  is  not  so  readily  derived.  If  the  artery 
is  emptied  by  compression  and  the  collapsed  vessel  palpated,  the  radial, 
if  normal,  is  barely  definable  as  a  separate  strand  ;  if  the  radial  is  thick- 
ened and  its  walls  stiff,  the  emptied  artery  is  palpable  below  the  point 
of  compression. 


POLYGRAPHIC  TRACINGS  21 

REFERENCES 
Chapter  III 

Foster's  Physiology,  Edition  1888,  Part  I. 

Gibson,  G.  A. :  Further  Observations  on  Heart  Block ;  British  Medical  Journal, 

1906,  II,  1113. 
Hirschfelder,  A.  D. :  Diseases  of  the  Heart  and  Aorta,  Edition  1910. 
Lewis,  T. :  Mechanism  of  the  Heart  Beat. 
Mackenzie,  T. :   Diseases  of  the  Heart,  Edition  1913. 
Marey,  B.  J.  :   Circulation  du  Sang. 
Morrow,  W.  S. :  Various  Forms  of  the  Negative  or  Physiological  Venous  Pulse ; 

British  Medical  Journal,  1906,  II,  1807. 
Ohm,  R. :   Venen  Puis  und  Herzschallregistrirung. 
Wiggers,  C.  J. :   Circulation  in  Health  and  Disease,  64. 


CHAPTER  IV 


THE  ELECTROCARDIOGRAM 


Fundamental  Physiological  Considerations.  —  The  electrocardio- 
gram is  based  upon  the  fundamental  physiological  fact  that  any  muscle 
upon  contracting  produces  a  definite,  though  minute  amount  of  elec- 
tricity. The  current 
thus  produced,  if  al- 
lowed to  pass  through 
a  sensitive  galvanom- 
eter, causes  deflection 
of  the  needle.  For  ex- 
ample, a  muscle  con- 
sisting of  parallel  fibers 
(Fig.  29,  M)  is  stimu- 
lated at  the  point  S, 
the  surface  at  that  area 
is  connected  by  means 
of  a  non-polarizable 
electrode  (Ei)  to  the 
galvanometer  (G),  and 
the  other  electrode  (E2) 
is  grounded  so  that  it 
remains  constant  (equi- 
potential) ;  then  the  muscle  at  S  in  contracting  becomes  electrically 
negative  relative  to  the  remainder  of  the  musculature.  As  the  current 
passes,  the  stimulated  end  becomes  quiescent ;  the  electropotential  falls 
and  reaches  zero ;  meanwhile  the  needle  of  the  galvanometer  is 
deflected  and  then  comes  to  rest.  If  recorded,  such  deflection  would 
be  a  monophasic  curve  (Fig.  29). 

If,  instead  of  being  grounded,  the  electrode  is  connected  with  the 
other  end  of  a  parallel  fibered  muscle  (Fig.  30,  E2)  and  the  latter  is 
stimulated  at  the  point  S  (Fig.  30),  the  stimulated  area  in  contract- 
ing becomes  electronegative,  the  other  areas  relatively  positive.  The 
current  flows  from  —  Ex  to   +  E2  (Fig.   30)  and  produces  a  current 

22 


Fig.  29.  —  Scheme  of  monophasic  action  current.  (Modi- 
fied from  Kraus  and  Nicolai — "Das  Elecktrokardio- 
gramm.") 

M  =  muscle  consisting  of  parallel  fibers  ; 
S  =  point  of  stimulation  ; 
Ei  =  non-polarizable  electrode  ; 
E2  =  earthed  electrode  ; 
G  =  galvanometer ; 
C  =  resultant  monophasic  curve. 


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THE   ELECTROCARDIOGRAM 


23 


in  the  galvanometric  circuit.  When  the  contraction  wave  arrives  at 
the  center  of  the  muscle,  no  current  is  induced  because  this  zone  draws 
negative  ions  in  equal  amounts  from  both  sides.  The  two  latter  being 
positive,  there  is  no  difference  in  po- 
tential and  the  needle  is  not  deflected. 
With  the  passage  of  the  contraction 
wave  toward  E2,  the  latter  becomes  elec- 
tronegative (the  negative  pole) ;  the 
current  now  flows  from  —  E2  to  +  Ei 
and  the  needle  is  deflected  in  the  op- 
posite direction.  In  other  words,  with 
change  in  electrical  signs  the  needle  is 
again  deflected  and  a  diphasic  curve 
results. 

In  view  of  later  electrocardiographic 
considerations,  it  is  important  to  em- 
phasize that  the  resultant  curve  depends 
upon  the  direction  of  the  contraction 
wave  in  the  muscle  and  upon  the  point 
at  which  the  contraction  arises.  It 
further  depends  upon  the  axis  of  the 
muscle  mass  in  relation  to  the  electrical 
wave.  It  is  also  evident  that  the  course 
of  the  contraction  wave,  of  the  galva- 
nometric deflections,  and  of  areas  of 
relative  negativity  are  intimately  corre- 
lated. These  simple  considerations  regarding  the  action  of  a  contract- 
ing muscle  upon  a  galvanometric  needle  will  serve  to  clarify  the 
principles  underlying  the  electrocardiographic  apparatus.  The  latter 
as  first  constructed  by  Einthoven  consists  essentially  of  a  fine  conduct- 
ing fiber  lying  in  a  narrow  space  between  two  approximated  poles 
of  a  powerful  electromagnet.  The  fiber  or  string  is  deflected  by  cur- 
rents induced  in  it.  The  string  is  so  sensitive  and  delicate  that  it  is 
deflected  by  very  weak  currents  drawn  from  the  surface  of  the  body. 
It  is  usually  made  of  an  exceedingly  fine  quartz  fiber  coated  with 
silver.  Its  thickness  varies  from  .002  mm.  to  .005  mm.,  its  resistance 
from  1500  to  7000  ohms.  The  electrocardiographic  apparatus  which  I 
use  —  a  standard  type  —  is  schematically  shown  and  described  in 
Fig.  31.     Figure  32  (Plate  II)  shows  the  apparatus  set  in  position. 

Method  of  taking  an  Electrocardiogram  —  the  Three  Leads  or 
Derivations.  —  There  are  various  methods  of  employing  non-polariz- 
able  electrodes  to  conduct  the  potential  produced  by  cardiac  activity  to 
the  galvanometer.  One  method  consists  in  wrapping  flannel  bandages, 
each  about  6  inches  wide  and  9  feet  long,  thoroughly  soaked  in  a  strong 
warm  salt  solution  (6  oz.  of  salt  to  one  pint  of  water),  around  each  fore- 
arm and  around  the  left  leg  of  the  patient.     After  these  extremities  have 


Fig.  30.  —  Scheme  of  diphasic  ac- 
tion current.    (Considerably  mod- 
ified from  Kraus  and  Nikolai.) 
Mu  =  parallel  fibered  muscle  ; 
C  =  center  point ; 
<S  =  point  of  stimulation  ; 

Ei,  Ei  =  non-polarizable  electrodes. 
Minus  signs  over  Mu  show  that 
that  area  has  become  electronega- 
tive when  reached  by  the  contrac- 
tion wave,  and  that  both  ends  are 
then  temporarily  positive.  (See 
text.) 


24 


CLINICAL  CARDIOLOGY 


been  covered  by  a  few  turns,  German  silver  electrodes  with  binding 
posts  are  included  in  the  folds  of  the  bandage.  These  electrodes  are 
6  inches  long  and  5  inches  wide  and  are  sufficiently  thin  and  pliable 
to  be  bent  and  snugly  applied.  When  patients  can  sit  up,  a  simpler 
and  more  expeditious  method  consists  in  having  three  separate  vessels 


Fig.  31.  —  Scheme  of  rheostat  and  connection  with  the  galvanometer. 

N,  S,  are  the  North  and  South  poles  of  the  electromagnet  activated  by  the  storage 
batteries  S.B.  The  latter  are  connected  with  the  street  current  for  recharging. 
Between  the  poles  of  the  magnet  lies  the  silvered  quartz  fiber  (the  string),  St. 

D.T.S  I  and  D.T.S  II  are  double  throw,  double  pole  switches. 

C.R  1,  C.R  2,  C.R  3  are  crank  rheostats;  each  crank  with  11  stops  (including  zero) 
arranged  in  banks  as  figured  ;  the  ohms  in  each  bank  in  multiples  of  10. 

S.R  is  a  shunt  rheostat. 

P  =  potentiometer. 

D.C  =  dry  cell  with  a  voltage  of  about  1.3  volts. 
Each  rheostat  has  a  separate  function.  The  resistance  of  C.R  1  is  thrown  in  so  that  when 
put  in  circuit  with  the  potentiometer  by  switch  D.T.S  I,  the  former  indicates  10°,  a 
specially  arranged,  arbitrary  figure  which  equals  one  milliampere.  C.R  1  is  also  in  circuit 
with  D.  T.S  II  connected  with  the  galvanometer.  C.R  2  is  used  to  test  the  deflection  time 
of  the  string  and  to  measure,  if  necessary,  the  patient's  resistance.  C.R  3  contains  four 
banks.  Each  stop  of  the  bank  marked  2  is  equivalent  to  one  millivolt,  and  is  used  for 
the  purpose  of  standardization.  The  shunt  rheostat  S.R  is  used  to  reduce  the  sensi- 
tiveness of  the  galvanometer. 
After  both  forearms  and  left  leg  of  the  patient  are  put  into  salt  solution  (see  text  and  Fig. 
33)  they  and  the  potentiometer  are  thrown  into  circuit  by  the  switches  D.T.S  II  and 
D.T.S  I  respectively.  The  shunt  rheostat  S.R  is  then  moved  successively  upon  the 
stops  in  the  direction  of  the  arrow.  The  string  moves  a  variable  distance  from  the  cen- 
ter with  each  stop.  It  is  brought  back  each  time  by  throwing  in  resistance  from  the 
banks  of  C.R  3.  Usually  resistance  from  bank  3  is  sufficient.  Occasionally  bank  4  is 
required.  Finally  the  tension  of  the  string  is  adjusted  and  standardized  by  its  milled 
screw,  so  that  a  millivolt  of  current  (C.  R  3,  bank  2)  causes  a  deflection  of  1  cm.  The 
movements  of  the  string  are  magnified  approximately  600  times  by  the  microscope 
(M.M)  and  then  photographed  upon  a  moving  photographic  film.  In  this  manner 
tracings  of  various  lengths  can  be  obtained.  This  is  an  important  consideration, 
especially  when  studying  cardiac  mechanisms  which  are  only  occasionally  abnormal. 
A  time-marker  crosses  the  field  every  one-fifth  second  and  this  serves  to  standardize 
events  of  the  cardiac  cycle. 


containing  strong  warm  salt-water  solutions.  In  each  vessel  is  placed 
a  porous  cup  containing  a  100  per  cent  zinc  sulphate  solution  and  a  zinc 
plate  with  a  binding  post.  Thus  electrical  connection  is  established  be- 
tween the  patient  and  the  electrocardiographic  apparatus  (Fig.  33, 
Plate  III).  In  either  case,  binding  posts  are  connected  by  wires, 
distinguished  by  varying  colors,  and  are  placed  in  circuit  with  the  gal- 
vanometer by  means  of  plugs  and  switches.     The  heart,  in  contracting, 


PLATE  III 


Fig.  33.  —  Photograph  of  patient  with  electrodes  connected  with  the  galvanometer. 


THE   ELECTROCARDIOGRAM 


25 


Fig. 


34.  —  Diagram  illustrating 
the  three  leads. 


gives  rise  to  waves  of  electric  potential  which  spread  from  their  source 
over  the  entire  body.  It  is  these  that  are  conducted  to  the  galva- 
nometer by  means  of  the  non-polarizable  electrodes.  There  are  thus 
three  arbitrary  directions  of  the  current  coursing  through  the  heart, 
which  correspond  to  the  three  extremities. 
These  are  the  so-called  "leads"  or  "deriva- 
tions." The  current  (Fig.  34)  from  the 
right  to  left  arm  (R.A-L.A),  running 
chiefly  across  the  base  of  heart,  is  the  first 
lead  or  derivation ;  that  from  the  right  arm 
(R.A)  to  the  left  leg  (L.L),  approximately 
parallel  to  the  long  axis  of  the  heart,  is 
the  second,  sometimes  called  the  "  strong  " 
lead;  that  from  the  left  arm  (L.A)  to  the 
left  leg  (L.L)  is  the  third  lead  and  draws 
off  the  current  coming  mainly  from  the  left 
side  of  the  heart. 

The  photographic  reproduction  of  the 
deflections  of  the  galvanometric  string  dur- 
ing the  registration  of  the  various  leads  constitutes  the  electrocardio- 
gram. While  the  electrocardiograms  of  no  two  persons  are  exactly 
alike  —  they  may  indeed  be  quite  dissimilar  —  and  while  physiological 
differences  vary  within  wide  limits,  there  is  a  general  conformity  to 
y=.^o  a  normal  type.     A  typical  normal 

electrocardiogram  is  schematically 
shown  in  Fig.  35,  which  represents 
the  various  waves  or  deviations, 
and  the  approximate  time  required 
for  each,  when  the  heart  is  beating 
rhythmically  at  the  rate  of  72  per 
minute.  Each  division  parallel  to 
the  base  line  (the  line  of  isopoten- 
tial)  is  equivalent  to  one  millivolt 
(10-4  volt).  The  electrocardiogram, 
that  is,  the  registration  of  the  dif- 
ference of  electric  potential,  pre- 
cedes the  actual  cardiac  contraction 
by  about  .03  second. 

The  Normal  Electrocardiogram. 
—  The  normal  electrocardiogram 
will  now  be  considered.  The  no- 
menclature I  shall  adopt  is  that 
first  introduced  by  Einthoven  and, 
with  few  exceptions,  now  in  general  use.  Following  the  sequence  of 
normal  cardiac  activity,  the  electrocardiogram  is  conveniently  divided 
into  that  produced  by  auricular  contraction,  —  the  auricular  complex, 


m 


~v~ 


SECOrODS    — 


TATE.     •      fZ     CEPSN1- 

Fig.  35.  —  Schematic  representation  of  a 
typical  electrocardiogram,  second  lead. 
Each  horizontal  space  measures  one  mil- 
livolt. The  ordinates  measure  one-fifth 
second.  The  form  and  size  of  the  va- 
rious deviations  are  seen,  as  well  as  the 
time  required  for  their  formation. 


26  CLINICAL  CARDIOLOGY 

—  and  that  by  ventricular  contraction,  —  the  ventricular  complex. 
Animal  experimentation  and  observations  on  the  human  subject  with 
normal  and  abnormal  rhythms,  especially  those  with  heart  block 
and  auricular  fibrillation,  have  confirmed  the  fact  that  the  auricular 
complex  (known  as  the  P  wave)  is  caused  by  auricular  contraction. 
This  wave  is  directed  upward,  that  is,  it  is  electrically  base-negative 
(base-active) ;  it  is  usually  somewhat  flattened  at  its  summit. 
After  reaching  the  base  line  it  is  succeeded  by  a  short  horizontal 
isoelectric  line,  an  evidence  of  quiescence  of  electric  potential.  The 
ventricular  complex  consists  of  the  QRST  deviations.  The  Q  and 
S  vary  in  size ;  they  are  usually  short,  sharp  peaks  directed  down- 
ward (electrically,  base-positive  or  what  is  the  same  thing,  apex- 
negative  or  -active,  "negativity"  and  "activity"  being  synonymous); 
they  may,  however,  be  absent.  Lewis  terms  all  downwardly  directed 
deviations  S  waves.  I  have  followed  Einthoven's  method  by  which 
the  direction  of  R  is  derived  from  the  formula  R  I  =  R  II  — R  III 
(Chapter  V).  Based  upon  the  electrophysiological  facts  already  de- 
scribed, this  appears  to  give  a  more  rational  and  less  arbitrary  reason 
for  the  names  of  the  different  ventricular  peaks.  The  R  deviation,  the 
most  prominent  of  all  the  waves  of  the  normal  electrocardiogram,  is 
directed  upwards  a  distance  varying  from  10  to  15  millivolts.  As 
measured  at  the  base  line,  the  time  required  for  its  formation  varies 
from  .02  to  .05  second.  Because  of  the  quick  deflection  of  the  string, 
the  R  deviation  appears  as  a  fine  line.  The  T  wave  slopes  gradually ; 
the  down  stroke  is  somewhat  thinner  than  the  upstroke,  the  summit 
is  broad  and  flattened.  The  R  and  T  waves  are  sometimes  called  the 
first  and  second  ventricular  spikes,  respectively.  The  U  wave  rises 
only  slightly  above  the  isoelectric  line ;  it  is  not  always  present.  All 
curves  are  taken  with  a  known  deflection  time  of  the  string.  The  latter 
is  determined  by  rapidly  throwing  in  and  cutting  out  a  millivolt  of 
current  with  the  string  tension  at  its  usual  standard  (Fig.  36,  Plate  IV). 
The  limit  of  accuracy  for  this  deflection  time  is  approximately  .02 
second  ;  when  slower,  the  string  registers  curves  inaccurately  flattened 
and  low. 

Variations  from  the  Normal  Type.  —  The  usual  variations  are  ab- 
sence of  the  U  wave ;  marked  differences  in  the  height  of  the  R  in  the 
several  leads ;  a  split  R  wave  with  thick  sides  or  summit ;  abnormally 
large,  flat,  or  diphasic  T  waves,  especially  in  leads  2  and  3 ;  a  low,  flat, 
or  split  P  wave  or  its  absence  in  one  of  the  leads ;  deep  Q  and  S  waves 
and  a  so-called  QRS  complex  (q.v.).  While  the  cause  of  some  of  these 
variations  is  known,  the  etiology  of  others  is  obscure  or  still  in  dispute. 

The  Normal  Electrocardiogram  and  its  Interpretation.  —  A  typical 
normal  electrocardiogram  —  three  leads  —  of  an  adult  with  a  normal 
heart  is  shown  in  Fig.  37.  The  R  deviation  is  tallest  in  the  second, 
the  "strong"  derivation  (Fig.  34),  which  leads  off  the  current  in  a  direc- 
tion parallel  to  the  long  axis  of  the  heart.     Certain  basic  facts  regarding 


THE   ELECTROCARDIOGRAM 


27 


Fig.  37.  —  Normal  electrocardiogram.  L  I,  L II,  L  III 
are  the  three  leads.  The  darker  shaded  ordinates 
measure  one-fifth  second.  The  horizontal  spaces,  one 
millivolt  each.  The  S  wave  is  scarcely  discernible  in 
L  III.  The  R  wave  is  tallest  in  L  II.  (Courtesy  of 
Dr.  A.  E.  Cohn.) 


the  electrocardiogram  are  necessary  to  the  reader  in  order  more  readily 
to  comprehend  the  difference  in  size  and  direction  of  the  deviations  in 
the  various  leads  in  normal  and  abnormal  hearts.  The  electrocardio- 
gram is  the  graphic  representation  of  the  spread  of  the  electrical  impulse 
throughout  the  heart. 
With  normal  cardiac 
rhythm,  the  peaks  or 
deviations  of  the  elec- 
trocardiogram represent 
at  any  instant  of  time 
the  total  differences  of 
electrical  potential.  The 
QRS  and  probably  the 
T  deviations  are  caused 
by  the  spread  to  both 
ventricles  of  the  excita- 
tion wave  along  the 
auriculo-ventricular  junc- 
tional tissue.  An  up- 
wardly directed  R  peak 
denotes  activity  of  the 
ventricular  base  relative 
to  the  remainder  of  the 
musculature.  The  course  and  the  spread  of  the  muscular  contraction 
and  of  the  electrical  excitation  waves  are  intimately  connected,  so  that 
activity  and  electrical  negativity  are  interchangeable  terms.  This 
may  be  proved  experimentally  by  placing  two  electrodes,  one  upon  the 
right  ventricle  in  front,  the  other  upon  the  apex ;  if  the  right  ventricle 
is  first  stimulated,  the  R  is  deviated  upward  (base-active) ;  if  the  apex, 
the  resultant  deviation  is  downward  (apex-active). 

Influences  Affecting  the  Electrocardiogram. — From  what  has  been 
said  regarding  monophasic  and  diphasic  curves  and  their  fundamental 
electrophysiological  causes,  it  is  evident  that  purely  physical  con- 
siderations affecting  a  contracting  —  and  therefore  an  electrically  ex- 
cited —  muscle  may  influence  the  resultant  electrocardiogram.  For 
example,  let  us  in  Fig.  30  conceive  the  muscle  to  consist  of  fibers  of 
various  lengths  running  in  various  directions,  instead  of  being  of  the 
same  length  and  parallel ;  we  should  then  expect  some  change  in  the 
electrocardiogram  from  the  original  simpler  conception.  If,  in  addi- 
tion, we  imagine  the  muscle  volume  so  changed  that  instead  of  an 
evenly  cut  straight  muscle  we  are  dealing  with  larger  and  smaller  ir- 
regular masses,  there  will  again  be  changes  from  the  original  monophasic 
curve.  These  physical  considerations  actually  apply  to  the  electro- 
cardiogram derived  from  the  human  heart. 

It  has  already  been  pointed  out  that  the  muscular  architecture  of 
the  heart  is  an  extremely  intricate  one,  and  that  there  are  layers  which 


28  CLINICAL  CARDIOLOGY 

run  in  various  directions  from  one  chamber  to  the  other  (Chapter  I). 
This  phase  of  pure  mass  consideration  as  affecting  and  influencing  the 
electrocardiogram  has  been  admirably  summed  up  by  A.  E.  Cohn  as 
due  to  the  "disposition  and  volume  of  the  muscular  mass  of  each  pair 
of  cavities."  Volumetric  and  mass  considerations  apply  not  only  to 
the  involved  architecture  of  the  normal  heart,  but  also  to  diseased  and 
hypertrophied  hearts.  For  example,  it  seems  probable  that  the  hyper- 
trophic process  does  not  always,  or  perhaps  not  even  regularly,  express 
itself  by  hypertrophy  of  one  chamber  as  compared  with  the  other,  but 
rather  as  a  process  affecting  the  fundamental  complicated  muscle  layers. 
Applying  these  considerations,  it  can  now  be  understood  how 
changes  in  muscular  volume  and  mass  profoundly  influence  the  size 
and  direction  of  the  electrocardiographic  deviations.  It  is  likewise 
evident  that  any  classification  based  upon  differences  of  disposition 
and  volume  of  the  cardiac  musculature  will  meet  with  numerous  ex- 
ceptions, the  causes  for  which  it  may  be  impossible  to  fathom.  Bearing 
these  limitations  in  mind,  the  following  tabulation  is  offered  in  an  attempt 
to  clarify  many  of  the  causes  for  variations  from  the  normal  electro- 
cardiographic standard. 

Disposition  and  Volume  of  the  Ventricular  Musculature  as  Affecting 
the  Electrocardiogram.  — 

A.  Horizontally  disposed  (squatty)  hearts. 

B.  Vertically  disposed  (drop)  hearts. 

C.  Cardiac  displacements. 

D.  Congenital  dextrocardia. 

E.  Phasic  variations  with  breathing. 

F.  Ventricular  hypertrophy  (left  and  right). 

G.  Ventricular  dilatation  (left  and  right). 

H.    Abnormal  rocking  motion  of  the  ventricle. 

A.  Horizontally  Disposed  (Squatty)  Hearts.  —  If  from  any  cause 
the  heart  lies  abnormally  flat  upon  the  diaphragm,  the  ventricles  are 
apt  to  be  '  disposed  '  with  a  preponderant  balance  to  the  left,  as  dia- 
grammatically  illustrated  in  Fig.  38,  D.  In  some  clinical  cases  of  squatty 
heart,  R  III l  is  either  dwarfed  or  negative. '  Leaving  the  question  of 
hypertrophy  for  later  consideration,  examples  of  squatty  hearts  are 
found  especially  in  obese,  middle-aged  individuals.  Electrocardio- 
grams from  several  such  patients  are  shown  (Figs.  39,  40,  41,  Plate  IV). 
Cardiac  symptoms  are  rarely  present.  Fluoroscopic  examinations  (Chap- 
ter IX)  reveal  the  ventricular  mass  lying  flat  upon  the  diaphragm ;  the 
dome  of  the  latter  is  less  curved,  and  the  diaphragmatic  excursion  is 
reduced  in  range.  These  factors  are  of  importance  in  the  etiology  of 
the  abnormal  position  of  the  ventricles.    Gaseous  distention  of  the  stom- 

1  The  numerals  placed  after  the  deviations  refer  to  the  latter  in  their  respective 
leads. 


PLATE   IV 


1 1  jllli 


Fig.  36.  —  Electrocardiogram  showing  the  deflection  time  of  the  string.     The  points 
A  and  B  are  about  .02  of  a  second  apart. 


1 


Fig.  39. 


-*:: 


FTT~~1 


-*iu— 


___        r .  _  - 


-:n 


=: 


Fig.  40. 


-♦• — '       ' ■  ■  ' 


Fig.  41. 

Fig.  38,  40,  41. — Electrocardiograms  of  patients  with  normal  hearts  and  with  negative 
R  in  L  III.     In  all  these  cases  the  ventricle  lay  flat  upon  the  diaphragm. 


THE   ELECTROCARDIOGRAM 


29 


NSSPirtM'io'vl 


Fig.  38.  —  Schematic  representations  showing 
leads   with   varying   ventricular   axes  and  th 
though   the  ventricles   are   schematically   of 
the  volumetric  contents  of  both  chambers  are 
A  =  normal  heart ; 
B  =  left  ventricular  dilatation  ; 
C  =  right  ventricular  dilatation  ; 
D  =  left  ventricular  hyperbalance  ; 
E  =  right  ventricular  hyperbalance  ; 
F  =  left  ventricular  hypertrophy  ; 
G  =  right  ventricular  hypertrophy  (elec- 
trocardiogram as  in  C)  ; 


the  angles  made  by  the  direction  of  the 
e   corresponding  electrocardiograms.     Al- 
different  sizes,  it  is  here  assumed   that 
alike. 
H  =  block  of  right  bundle  branch  ; 
/  =  block  of  left  bundle  branch  ; 
J  =  left  ventricular  extrasystole  : 
K  =  right  ventricular  extrasystole; 
L  =  change  of  position  of  the  heart  with 
inspiration  and  expiration. 


30 


CLINICAL   CARDIOLOGY 


ach  may  have  a  similar  effect  upon  the  position  and  action  of  the  dia- 
phragm, and  hence  upon  the  position  of  the  heart. 

B.  Vertically  Disposed  (Drop)  Hearts.  —  Quite  opposite,  theoretically, 
to  the  foregoing  is  the  distribution  of  the  ventricular  musculature  when 
the  heart  is  narrow  and  lies  vertically  in  the  chest.  The  assumed  muscular 
axis  is  then  diagrammatically  represented  in  Fig.  38,  E;  R  I  becomes  ab- 
normally small  or  negative.  Clinically,  patients  with  vertically  directed 
(so-called  "drop")  hearts  are  apt  to  be  young,  tall,  and  gaunt  individ- 
uals with  loosely  hung  hearts.  With  the  fluoroscope  (Chapter  IX)  the 
entire  organ  appears  narrow  and  graceful,  and  for  the  most  part  hidden 
behind  the  sternum.  At  times,  the  apex  scarcely  touches  the  diaphragm. 
An  illustrative  electrocardiogram  is  shown  in  Fig.  42  (Plate  V). 

C.  Cardiac  Displacements.  —  The  heart  can  be  displaced,  as  is 
known,  by  pleural  exudates,  adhesions,  mediastinal  tumors,  etc.  If 
the  heart  is  displaced  laterally  so  that  there  is  no  disturbance  of  the 


\       1 

\     . 


Fig.  43. — Orthodiascopic  tracing  of  heart  of 
normal  child  lying  on  its  back  (A),  left  (B), 
and  right  (C)  side,  respectively. 


PLATE   V 


m 


Fig.  42. —  Electrocardiogram  of  patient  with  narrow  heart  ("drop"  heart)  illustrating 
right  ventricular  hyperbalance. 


-- 


n:^U 


■1 


,3 

4k  .1        V' 

I 


^m/1***.* 


Fig.  45.  —  Electrocardiogram  of  a  child  whose  ortho- 
diascope tracing  is  Fig.  148.  The  letters  A,  B,  and 
C  again  refer  to  the  position  of  the  child  on  its  back, 
left  and  right  sides  respectively. 


r     i 

c 

I 

i 


m\J 


' 

• 

'V 

- 

.  

__- 

::  _: 

~  n  zz 

-_l_. 

_z 

■■   -■ 

- -_--- 

-- 



-f  ■ 

_^ 

~a+r:r 

lipi 

w 

Lr 

i 

-  — 1 

r  nl  r 

i  t~i  1  i~- 

i  it  t  r 

4-4- 

Fig.  48.  —  Slight  phasic  variation  with  breathing. 


' 4. L L J_  4 j 1_ 


£-• 

IU 

m 

Vl 

; 

^ 

■ 

i 

m 

Mr 

4 

+._ 

Fig.  47.  —  Acquired  dextro- 
cardia with  normally  di- 
rected deviations  in  all 
three  leads. 


-j_- 

= 

F 

— 

•• 

--— 

wb 

- 

i 

~n~  " 

3E 

1      T  n  - 

Fig.  49— Li/.   Slight  phasic 
variation  with  breathing. 


THE   ELECTROCARDIOGRAM 


31 


Fig.  44.  —  Orthodiascopic  tracing  of  normal  child 
lying  on  its  back  (A),  left  (B),  and  right  side  (C), 
respectively. 

muscular  balance  of  the  heart,  the  electrocardiogram  does  not  change. 
The  latter  is  only  affected  when  the  changes  in  the  cardiac  position 
cause  a  change  of  the  plane  of  electrical  potential  in  relation  to  the 
fixed  body  planes  (represented  by  the  "leads").  The  effect  of  dis- 
placement can  be  best  exemplified  in  children,  and  is  illustrated  in  Fig. 
43,  A,  B,  C,  which  are  the  orthodiascopic  tracings  of  a  healthy  boy  of  ten 
lying  alternately  on  his  back,  left  and  right  sides.  The  tracings  show 
marked  variations  in  the  disposition  and  contour  of  the  heart,  mainly 
due  to  ventricular  rotation  and  consequent  foreshortening  or  lengthening 
of  the  cardiac  outline.  Another  illustration  of  a  mobile  heart  is  Fig.  44 
(positions  A,  B,  C),  orthodiascopic  tracings  of  the  normal  heart  of  a  child 
of  seven  lying  alternately  on  her  back,  left  and  right  sides.  Correspond- 
ing electrocardiograms  were  taken  (Fig.  45,  Plate  V,  A,  B,C).  In  addi- 
tion to  slight  changes  in  the  Q  and  S  deviations,  the  heights  of  the  R  in 
the  A,  B,  C  positions  varied  as  follows :  Lead  I,  R  =  6A,  5B,  6C  (the 
numbers  refer  to  the  number  of  millivolts  of  deflection) ;  in  Lead  II, 
R  =  10A,  15B,  16°;   in  Lead  ///,  R  =  6A,  13B,  10c. 

D.  Congenital  Dextrocardia.  —  As  a  corollary  to  the  observations 
already  made  regarding  the  effect  of  change  of  the  planes  of  electrical 
potential  upon  the  electrocardiogram,  it  is  apparent  that  congenital 
dextrocardia  in  the  first,  sometimes  called  the  symmetrical  lead,  will 


32 


CLINICAL  CARDIOLOGY 


produce  electrocardiographic  deviations  exactly  opposite  in  direction 
to  the  normal  (Fig.  46).  All  the  peaks  are  directed  downwards  instead 
of  upwards ;  R  III  becomes  taller  than  R  II.  Such  an  electrocardio- 
gram offers  indubitable  proof  of  congenital  dextrocardia  and  serves  to 
distinguish  the  latter  from  acquired  right-sided  malpositions  of  the 
heart  due  to  fluid  in  the  chest,  pulmonary  tumors,  pneumothorax,  adhe- 
sions, etc.  For  example,  Fig.  47  (Plate  V)  is  the  electrocardiogram  of 
a  patient  with  an  acquired  dextrocardia,  in  whom  the  heart  was  drawn 
into  the  right  chest  by  adhesions  following  a  right-sided  pulmonary 
abscess  and  subsequent  pleural  fistula  following  operation.  Fluoro- 
scopically,  the  heart  was  seen  to  occupy  an  area  in  the  right  chest  prac- 


s 

u 

BWj 

rt4+ 

IrH-H 

44444-1 

►" |T 

tK 

n 

tit 

jLa- 

"_ 

+t 

HU 

44444 

jut 

• 

Fig.  46. 


Congenital  dextrocardia.     All  the  deviations  are  directed  downwards,  in  L  I. 
R  III  is  taller  than  R  II. 


tically  identical  with  that  of  congenital  dextrocardia.  Since  the  heart 
had  been  pulled  in  a  lateral  direction  only,  the  electrocardiographic  de- 
viations remained  normal  in  direction. 

E.  Phasic  Variations  with  Breathing.  —  As  the  result  of  breathing, 
some  electrocardiograms,  usually  in  the  second  and  third  leads,  present 
a  rhythmic  waxing  and  waning,  an  increase  and  decrease  in  the  size  of 
the  jR  waves.  During  fluoroscopy,  I  have  often  noted  a  marked  varia- 
tion in  the  position  of  the  heart  during  respiration  (Fig.  38,  L) ;  it  is 
sometimes  sufficiently  pronounced  to  produce  a  movement  of  the  apical 
portion  of  the  ventricle  through  an  arc  of  several  centimeters.  This 
shift  is  most  evident  in  younger  individuals  with  thin  chest  walls  and 
large  respiratory  excursions  of  the  diaphragm ;  it  is  least  in  patients 
with  fat  abdominal  walls  and  broad  hearts.  The  heart  moves  with  the 
base  as  a  comparatively  fixed  point.  During  inspiration  there  is  a 
descent,  in  a  clockwise  direction,  of  the  ventricular  mass,  especially 
of  its  apical  portion.  The  heart  tends  to  assume  an  erect  position. 
The  rise  of  the  diaphragm  during  expiration  produces  a  contrary  effect ; 
the  left  ventricle  then  moves  anti-clockwise.  These  movements,  when 
extreme,  necessarily  affect  the  muscular  disposition  of  the  ventricles 
and  alter  the  electrocardiogram.  This  is  usually  most  noticeable  in  the 
third  lead,  probably  because  the  left  ventricle  is  especially  influenced 
by  the  respiratory  phases.  R  III  becomes  taller  during  inspiration 
and  smaller  during  expiration  as  the  ventricular  mass  tends  to  assume 
a  more  vertical  or  horizontal  position,  respectively  (Fig.  38,  L). 


PLATE  VI 


Fig.  50.  —  Marked  phasic  variation  with  breathing. 


•if 

hi 

m 

faSyW^f 

■ 

Fig.  52.  —  Aortic  stenosis.  Left  ventricular  hypertrophy. 
Negative  R  in  L  III.  Ventricular  extrasystole  {Ex)  in 
lead  III. 


Fig.  53.- — Negative  ventricular  deviation  III.    From  a  case 
of  left  ventricular  hypertrophy  and  aortic  aneurism. 


Fig.  51.  —  Aneurismal  dila- 
tation of  the  aorta  with 
left  ventricular  hyper- 
trophy.    Negative  R  III. 


t 


Fig.  55.  —  Electrocardiogram  of  a  boy  of  17  with  congenital 
ductus  arteriosus.  Note  negative  R  I,  R II,  evidence 
of  marked  right  ventricular  hyperbalance. 


^•V^w'yS,, 


Fig.  54.  —  Electrocardiogram  of  a  patient  with  aortic  regurgitation  and  left  ventricular 
hypertrophy ;   the  R  deviation  is  positive  in  LIII. 


THE   ELECTROCARDIOGRAM 


33 


l|!!;i|! jMimH  jfr 

— 

— 

:    i  iu 1:J {-.i-'J-i .     '1   '■     ',i   II1'1- 

r* 

1 

— 

-  ...  yp......  ^jp^ 

th ,  1 1 1  ■ "  h  "i 

1 

, 

^ 

-1 

Fig.  48. 


-L  III.     Phasic  variation  with  breathing. 
difference  in  size  of  the  R  deviations. 


Note  the 


Respiratory  phasic  variations  are  also  found  in  patients  with  ven- 
tricular hypertrophy,  but  the  cardiac  excursion  being  ordinarily  less,  the 
phasic  electrocardi- 
ographic variations 
became  correspond- 
ingly limited.  Fig- 
ures 48  and  49 
(Plate  V)  are  ex- 
amples of  a  mod- 
erate respiratory 
effect  upon  the  size  of  the  deviations.  Figure  48  is  the  electrocardio- 
gram of  a  stout  individual  with  a  normal  heart  lying  in  a  squatty 
position;  Fig.  49,  from  a  patient  with  left  ventricular  hypertrophy. 
When  R  III  is  small,  phasic  variations  may  not  only  dwarf  it  but  cause 
its  final  disappearance,  as  shown  in  Fig.  50  (Plate  VI). 

F.  Ventricular  Hypertrophy  —  Left  and  Rigid  (Fig.  3S,F,G). —  It 
has  sometimes  been  assumed  that  negative  R  I  and  positive  R  III,  and 
positive  It  I  and  negative  R  III,  are  always  indicative  respectively  of 
right  and  left  ventricular  hypertrophy.  This  observation  has  been 
partly  substantiated  by  necropsies.  On  the  other  hand,  exceptions 
have  been  noted  both  at  post  mortem  and  as  the  result  of  clinical  ex- 
amination. Some  undoubted  cases  of  left  ventricular  hypertrophy, 
for  example,  do  not  give  the  deviations  assumed  for  this  condition.  In 
addition,  it  is  by  no  means  infrequent  to  find  patients  with  perfectly 
normal  hearts,  resting  normally  "disposed"  in  the  chest,  who  present 
the  deviations  supposedly  typical  of  hypertrophy.  It  will  thus  be  seen 
that  there  are  many  drawbacks  and  exceptions  to  definite  conclusions 
regarding  the  existence  of  hypertrophy  based  upon  the  direction  of  the 
electrocardiographic  deviations.  As  a  general  rule,  however,  it  will 
be  found  that  in  aortic  disease  with  evident  left  ventricular  prepon- 
derance, R  I  is  positive  and  R  III,  negative.  Examples  are  given  in 
Figs.  51  and  52  (Plate  VI)  and  in  Fig.  53.  Occasionally,  however, 
RIII  is  positive,  even  when  left  ventricular  hvpertrophy  is  present 
(Fig.  54,  Plate  VI). 

The  electrocardiographic  evidence  of  right  ventricular  hypertrophy 
is  best  exemplified  by  congenital  cardiac  disease  due  to  malformation 
of  the  pulmonary  artery.  This  is  illustrated  by  the  case  of  a  boy  of  17 
with  patent  ductus  arteriosis  (Fig.  55,  Plate  VI).  Both  R  I  and  R II 
are  negative.  Upon  the  theory  of  mass  imbalance  affecting  the  electro- 
cardiogram, it  would  seem  that  together,  negative  R I  and  R II  are  in- 
dicative of  very  marked  right  ventricular  hypertrophy.  The  same 
theoretical  consideration  applies  to  negative  R  II  and  R  III  as  indicating 
extreme  left  ventricular  hypertrophy,  as  exemplified  in  Fig.  56  (Plate 
VII),  taken  from  a  patient  with  aortitis,  and  clinical  and  fluoroscopic 
evidence  of  extreme  left  ventricular  hypertrophy.  Infants  and  young 
children  are  also  apt  to  have  the  electrocardiographic  complex  of  right 


34 


CLINICAL  CARDIOLOGY 


ventricular  enlargement,  because  in  them  the  walls  of  the  right  ventricle 
are  relatively  thick. 

Cases  of  mitral  stenosis  do  not  always  yield  electrocardiograms  in- 
dicative of  right  ventricular  hypertrophy,  a  condition  usually  associated 
with  this  lesion.  Thus,  Figs.  57  and  58  are  from  cases  of  marked  and 
typical  stenoses.  In  Fig.  57,  the  main  ventricular  deviation  is  negative. 
The  R  deviations  in  Fig.  58  are  positive.  Whether  the  latter  and  sim- 
ilar apparently  atypical  electrocardiograms  in  cases  in  whom,  clinically, 
right  ventricular  hypertrophy  is  assumed,  are  due  to  some  of  the  factors 
already  discussed  (abnormally  disposed  ventricles,  ventricular  dilatations 
or  hypertrophy)  or  whether  they  may  even  be  due  to  counterbalancing 
left  ventricular  hypertrophy,  it  is  at  present  impossible  to  state. 

G.  Ventricular  Dilatation  (Fig.  38,  B,  C). — Though  hearts  which 
are  organically  sound  may  occasionally  become  dilated  as  the  result  of 

overstrain  or  of  tachycardial  attacks, 
the  term  ventricular  dilatation  is  here 
meant  to  apply  to  decompensated,  dis- 
eased hearts.  To  a  great  extent,  our 
clinical  knowledge  regarding  cardiac 
dilatations,  especially  of  one  chamber  as 
contrasted  to  the  other,  or  of  dilatations 
as  differentiated  from  moderate  hyper- 
trophy, is  meager.  There  exists,  how- 
ever, some  definite  evidence  that  cardiac 
dilatation  following  acute  endocarditis  is 
not  uncommon  in  children.  This  subject 
has  never  been  studied  from  the  electro- 
cardiographic aspect,  but,  as  with  con- 
siderations regarding  the  effect  of  mass 
changes,  it  seems  probable  that  muscular 
redistribution  resulting  from  dilatation 
can  also  bring  about  changes  in  the  elec- 
trocardiographic deviations. 

H.  Abnormal  Rocking  Motion  of  the 
Ventricle. — During  the  course  of  routine 
fluoroscopic  examination  of  normal  and 
abnormal  hearts,  I  have  encountered  oc- 
casional cases  in  which  there  was  a  sort 
of  to-and-fro,  rocking  motion  of  the  ventricular  mass,  with  the  base  of 
the  heart  acting  as  the  fixed  area.  At  times  the  entire  mass,  at  others 
only  its  apical  portion,  was  seemingly  involved  in  this  abnormal 
motion.  It  is  possible  that  this  abnormal  motility,  whatever  its  cause, 
when  sufficiently  marked  to  disturb  muscular  mass  relations,  may  well 
produce  a  change  in  the  electrocardiogram.  Its  mechanism  may  be 
compared  to  that  causing  phasic  variations  with  breathing  (q.v.).  In 
the  latter,  however,  the  motion  is  comparatively  gentle  and  slow  and 


Fig.  57.  —  Advanced  mitral  ste 
nosis.  R I  is  negative.  Aurieu 
lar  fibrillation  is  present. 


PLATE  VII 


m 


& 


d 


i 


Fig.  56.  —  Electrocardiogram  showing  an  interpolated  extrasystole  (L  II,  Ex).  R  is 
abnormally  wide,  especially  in  LI  and  LIII.  The  direction  of  the  R  deviations 
in  the  various  leads  indicates  marked  left  ventricular  hypertrophy.  TI  and  Til  are 
negative,  presumed  evidence  of  myocarditis.  (From  a  patient  with  left  ventricular 
hypertrophy  and  luetic  aneurismal  dilatation  of  the  entire  thoracic  aorta.) 


■ 1    |  |  |  M —  " 


m 


Fig.  59.  —  Electrocardio- 
gram showing  somewhat 
thickened  R  summit. 


Fig.  60.  —  Electrocardiogram 
(L  II)  showing  slightly 
notched  R  summit. 


Fig.  61.  — -  Electrocardio- 
gram showing  split  R 
(M  complex). 


, 

-    | 

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'     (J' 

-11 

*H 

G  v 

^L 

m 

i 

yw    \*tir 

*  Jf 

•         ' 

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Ipjw^'™ 

1 "    i       i       i       i       i  -     i 

i 

Figs.  62,  63.  — Electrocardiograms  showing  split  R  (W  complexes). 


4  r*«r**  ******  mim&  M 


^J5i.^i!H!.:i5T..VVLJI.VvL.Jaia44_ 


U^-^/^^^p-w 


•rww  pjtww  www  hp  v  p  .v^rw  wvw 
} *  f|  '/     ■"-  '/  1  «/ 


Fig.  65.  —  Electrocardiogram  showing  intraventricular  block.  (Courtesy  of  G.  C.  Robin- 
son :  Archives  of  Internal  Medicine,  1916,  XVIII,  845.)  Note  the  notched  and  splintered 
complexes. 


: -f— 

. 

tl 

~ 

k 

Ipjf 

■  ii  1 

■1 

3» 

••• 

. 

i 

r 

IE 

Si 

p 

}l 

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; 

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i. 

i 

1 

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*= 

~l     Jl— J 

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Fig.  66.  —  Electrocardiogram  showing  ventricular  complexes  of  abnormal  width,  but  of 

normal  form. 


THE   ELECTROCARDIOGRAM 


35 


is  not  followed  by  a  second  rocking  motion,  which  is  characteristic  of 
the  to-and-fro  motion  alluded  to. 

The  possible  effects  of  this  type  of  abnormal  motility  will  be  men- 
tioned in  connection  with  the  M  and  W  complexes  (q.v.). 

Asynchronous  Auricular  and  Asynchronous  Ventricular  Activity  — 
Split,  Splintered,  and  Notched  R  and  P  Deviations,  and  M  and  W  Com- 
plexes. —  In  addition  to  variations  in  the  electrocardiogram  due  to 
disposition  and  volume  of  the  ventricular  musculature,  in  which  physio- 
logical synchronous  activity  of  the  chambers  has  been  assumed,  there 
are  conditions  in  which,  for  various  reasons,  there  is  a  retardation  of 
the  excitation  wave  in  one  chamber  as  compared  with  its  fellow.  This 
is  seemingly  responsible,  in  the  main,  for  many  of  the  "  split "  and 
"  notched  "  complexes. 

The  normal  difference  in  contraction  time  between  the  two  ventricles 
may  amount  to  as  much  as  .03  second.  If  there  is  a  slight  retardation 
of  the  excitation  waves  in  the  ventricles,  due  to  abnormal  ventricular 


Fig.  5S.  —  Advanced  mitral  stenosis  with  auricular  fibrillation.     All  the  R  deviations 

are  positive. 

asynchronism,  it  may  account  for  the  thickening  of  the  R  deviation  at 
its  summit  (Fig.  59,  Plate  VII).  It  may  also  account  for  various  degrees 
of  notching  at  the  apex  (Fig.  60,  Plate  VII).  If  the  notching  is  extreme, 
there  is  a  sharp  division  of  the  R  peak  into  two  similar  components. 
When  the  latter  are  directed  upwards,  the  complex  resembles  the  letter 
M.  The  letter  M  is  an  appropriate  term,  I  believe,  for  this  composite 
wave  (Fig.  61,  Plate  VII).  When  the  components  are  directed  down- 
wards, the  complex  resembles  the  letter  W  (Figs.  62,  63,  Plate  VIII). 

Some  of  the  complexes  which  I  have  termed  M  and  W  have  been 
called  the  QRS  complex  by  Lewis.  Because  of  the  similarity  of  their 
components,  many  of  these  seem  composed  of  two  separate  R  devia- 
tions with  or  without  Q  and  S  deflections.  The  M  and  IV  complex 
may  be  assumed  to  be  due  to  asynchronous  ventricular  contractions  if 
the  outlines  of  the  waves  are  sharp,  and  if  when  measured  at  their  base 
lines,  they  consume  not  more  than  twice  the  time  required  for  the  normal 
R  deviation ;  that  is,  a  basic  width  of  the  M  or  W  of  about  .06  of  a  second. 
(See  Intraventricular  Block.)  Even  when  the  individual  deviations 
are  small,  the  resemblance  to  the  letters  M  and  W  is  sufficiently  accurate 
to  warrant  their  descriptive  use,  especially  when  qualified  as  "  dwarfed," 


36 


CLINICAL   CARDIOLOGY 


"  flat,"  or  "  low."  These  letters  may  thus  serve  to  distinguish  and 
separate  many  of  the  electrocardiograms  found  in  the  heterogeneous 
and  somewhat  confused  QRS  groups.  While  many  of  the  M  and  W 
complexes  are  probably  due  to  ventricular  asynchronism,  it  seems  pos- 
sible that  the  to-and-fro  ventricular  motion  already  described  (q.v.) 
may  also  be  productive  of  similar  complexes;  or  even  that  a  sharp 
twist  of  the  ventricles  during  contraction  may  disturb  ventricular  mass 
relations  and  produce  a  deep  Q  or  S  wave.  I  have  observed  fluoroscopi- 
cally  several  instances  of  ventricular  rocking  motion  accompanied  by 
M  or  W  complexes,  or  deep  Q  and  £  waves. 

Similar  in  etiological  significance  to  the  notched  R  are  the  notched 
or  split  P  deviations  (Fig.  64)  which  occasionally  give  rise  to  the  appear- 
ance of  two  distinct  undula- 
tions. Such  complexes  are 
probably  due  to  asynchronous 
auricular  contractions.  A 
notched  P  is  found  most  often 
in  mitral  stenosis. 

Intraventricular  Block.  — 
Recently,  Oppenheimer  and 
Rothschild  have  described  a 
QRS  complex  in  which  the 
time  required  for  the  com- 
pletion of  this  group  was  pro- 
longed beyond  0.1  second,  ap- 
proximately the  normal  limit. 
The  R  wave  was  abnormally 
broad ;  instead  of  clean  and 
sharp  sides,  it  was  slightly 
or  considerably  notched  and 
broken.  The  waves  were 
usually  of  low  amplitude  in 
all  leads.  These  observers  found  this  electrocardiographic  complex 
in  cases  in  which  there  was  marked  arteriosclerotic  or  cardiovascular- 
renal  disease,  usually  associated  with  severe  myocarditis.  In  four 
cases  they  were  able  to  corroborate  the  clinical  picture  by  necropsy 
examination;  this  showed  sclerosis  especially  in  the  endocardial  and 
subendocardial  layers ;  that  is,  in  the  neighborhood  of  the  terminal 
arborizations  of  the  conduction  system.  They  believe  the  abnormal 
electrocardiogram  is  the  result  of  intraventricular  block,  thus  inter- 
fering with  the  normal  and  orderly  spread  of  the  electrical  excitation 
wave  throughout  the  heart.  It  should  be  pointed  out,  however,  that 
hearts  presenting  the  above  clinical  or  pathological  picture  need  not 
necessarily  produce  the  abnormal  electrocardiogram  described. 

G.  S.  Robinson  has   also   reported  a  series   of   cases  whose  QRS 
complexes  required  .10  or  longer  for  their  completion  (Fig.  65,  Plate  VII). 


Fig.  64.  —  Notched  P  wave  from  a  case  of  mitral 
stenosis.     (Courtesy  of  Dr.  A.  E.  Conn.) 


PLATE  VIII 


'-; 


■■ 


ii  || 


f 

■-fi 


Fig.  67. 


»JJ 


Fig.  68. 


1  -  ■  I  •**?• 


:'      1 


Fig.  69. 

Figs.  67,  68,  69.  —  Electrocardiograms  showing  ventricular  complexes  of  abnormal  width 
but  of  normal  form.     R  is  not  abnormally  wide  in  all  leads. 


P. 

I       11. 

$Ma 


\n 


...  * 


/' 


:r 


A 


*r« 


Fig.  73.  —  Electrocardio-      Fig.    74.  —  Electrocar-      Fig.   75.  —  Negative    T  HI.       From  a 
gram  showing  tall  Til.  diogram    showing    T  case  of  aortic  stenosis  with  left  ventric- 

taller  than  R.  ular  hypertrophy. 


THE   ELECTROCARDIOGRAM  37 

These  were  likewise  assumed  to  be  due  to  derangement  of  intraventri- 
cular conduction  from  hindrance  to  the  excitation  wave,  either  along  the 
normal  paths  or  at  the  normal  rate.  In  most  of  the  cases  from  whom 
the  electrocardiograms  were  taken  there  was  clinical  evidence  of  a  pro- 
found disturbance  in  the  muscular  efficiency  of  the  heart. 

The  "Wide  R." — Both  of  the  above  types  of  intraventricular  block 
are  characterized,  as  has  been  stated,  by  a  broken  and  notched  complex 
comprising  the  QRS  group.  In  an  entirely  different  category  belong 
those  cases  that  I  have  studied,  in  whom  the  R  deviations  are  normal 
in  shape  and  form,  whose  sides  are  unbroken  and  not  notched,  and  in 
whom  there  was  no  evidence  of  a  bundle  branch  lesion.  The  char- 
acteristic of  my  cases  was  the  abnormal  length  of  time  required  for  the 
completion  of  the  main  ventricular  wave.  The  normal  time  for  the 
completion  ot  the  latter  varies  from  .02  to  .05  second.  I  have  adopted 
as  a  standard  a  width  of  .07  or  over  as  being  an  "abnormally  wide  i?." 
A  few  cases  with  their  electrocardiograms  are  herewith  epitomized  :  Fig. 
56  (Plate  VII)  is  from  a  patient  who  had  general  anasarca  from  luetic 
cardiosclerosis.  R  I  =  .12  second,  R  II  =  .07,  R  III  =  .13.  Figure  66 
(Plate  VII)  is  from  a  case  of  dilatation  of  the  arch  of  the  aorta  and  mod- 
erate left  ventricular  hvpertrophv ;  the  clinical  diagnosis  was  cardioscle- 
rosis. R  I  =  .12,  R  III  =  .08."  Figure  67  (Plate  VIII)  is  from  a 
physician  of  53  who  developed  scarlatinal  nephritis  at  the  age  of  15.  At 
present  the  urine  contains  albumen  and  casts.  The  patient  has  the  phys- 
ical signs  and  symptoms  of  moderate  cardio-nephritis.  R  I  and  R  II 
each  equals  .07.  Figure  68  (Plate  VIII)  is  from  a  woman  of  68  who, 
when  first  seen,  was  suffering  from  anasarca  from  cardiovascular-renal 
disease.  Under  proper  therapy,  she  improved  remarkably.  R  I  =  .09. 
Figure  69  (Plate  VIII)  is  from  a  male  patient  of  55  suffering  from  hyper- 
tension and  moderate  cardiosclerosis.  R  I  =  .07.  The  electrocardio- 
grams of  all  these  patients  were  taken  during  the  stage  of  compensation. 

In  all,  I  have  observed  18  cases  which  presented  an  R  width  of  .07 
of  a  second  or  over.  All  of  these  cases  showed  unmistakable  signs  of 
severe  cardiac  disease,  and  at  one  time  or  another  were  decompensated. 
Clinically,  most  of  the  cases  had  hypertension  and  left  ventricular 
hypertrophy.  Myocardial  insufficiency  alone  was  not  the  cause  of  the 
abnormally  wide  complex,  for  most  of  the  electrocardiograms  were 
taken  when  symptoms  of  decompensation  were  slight  or  absent. 
Ventricular  dilatation,  another  possible  assumption  for  the  abnormally 
wide  R,  can  also  probably  be  disregarded  for  the  same  reason.  Be- 
sides, in  a  series  of  decompensated  valvular  cases  that  I  observed  in 
whom  ventricular  dilatation  was  a  marked  feature,  the  R  complexes 
were  of  normal  width. 

Although  the  fundamental  cause  of  the  wide  R  in  my  cases  is  not 
apparent,  it  is  probably  due  either  to  delay  in  the  development  of 
electrical  excitation  or  to  delay  in  its  propagation.  Since  the  complexes 
are  normal  in  form,  the  excitation  wave  has  apparently  followed  a 


38  CLINICAL  CARDIOLOGY 

normal  path  in  the  ventricles.  Delayed  propagation  seems  the  more 
probable  factor.  As  in  intraventricular  block,  severe  cardiosclerotic 
disease  is  assumed  to  cause  the  notched  and  delayed  QRS  complex, 
a  wide  7?  of  normal  shape  but  of  abnormal  width  may  conceivably  be 
due  to  patches  of  myocardial  thickening  scattered  throughout  the 
ventricular  wall  in  amounts  sufficient  to  impede  and  abnormally  prolong 
the  excitation  wave. 

It  should  be  mentioned  that  I  have  studied  the  complexes  of  other 
cardiovascular  cases  who  were  clinically  as  ill  as  the  "  wide  R  "<cases 
but  who  presented  no  abnormally  broad  complexes.  The  reason  for 
this  I  have  not  been  able  to  discover. 

Of  the  18  cases  studied,  the  R  complex  was  rarely  abnormally  broad 
in  all  leads.  Since  the  first,  second,  and  third  leads  draw  off  the  cardiac 
current  from  various  directions,  —  namely,  breadthwise,  diagonally,  and 
lengthwise,  respectively,  —  one  may  at  least  hypothesize  that  the 
diseased  myocardium  lay  chiefly  in  one  cardiac  plane,  thus  producing 
a  wide  R  in  the  corresponding  lead.  In  a  general  way,  those  cases 
which  clinically  showed  the  most  myocardial  disease  were  the  ones  in 
whom  the  R  complex  was  widest. 

REFERENCES 
Chapter  IV 

Carter,  E.  P. :   Clinical  Observations  on  Defective  Conduction  in  the  Branches 

of  the  Auriculo-ventricular  Bundle ;    Archives  of  Internal  Medicine,  1914, 

XIII,  803. 
Cohn,  A.  E.  :   Present  Status  of  the  Electrocardiographic  Method  in  Medicine ; 

Association  of  American  Physicians,  May  11-13,  1915;   American  Journal 

of  the  Medical  Sciences,  1916'  CLI,  529. 
Cohn,  A.  E.,  and  Lewis,  T.  :   Fibrillation  and  Heart  Block;   Heart,  1912,  IV,  15. 
Einthoven,  W. :    Le  Teleeardiogramme ;    Archives  Internationales  de  Plrysio- 

logie,  1906,  IV,  Fasc.  II,  132. 
Einthoven,  W. :    Xeuere  Ergebnisse  auf  dem  Gebiete  der  thierischen  Elektrizi- 

taet ;    Gesellschaft  deutseher  Naturforscher  und  Aertzte,  Verhandlungen, 

1911,  3. 
Einthoven,  W. :    Ueber  die  Deutung  des  Electrocardiograrnmes  ;  Archives  fuer 

die  gesammte  Physiologic  1912,  CXLIX,  65. 
Eppinger,  H.,  and  Rothberger,  C.  J.  :  Ueber  dieFolgen  der  Durchschneidung  des 

Tawarasehen  Sehenkels  des  Reitzleitungssystems. 
Hoffmann,  A. :  Die  Elektrocardiographie  als  Un'tersuchungsmethode  des  Herzens 

und  ihre  Ergebnisse.     Ed.  1914. 
Kraus,  F.,  and  Xicolai,  G. :  Das  Elektrokardiogramm  des  gesunden  und  kranken 

Menschen,  1910. 
Lewis,  T.,  and  Gilder,  M.  D.  D. :  The  Human  Electrocardiogram,  A  Preliminary 

Investigation,  etc. ;    Philosophical    Transactions  of  the  Royal    Society  of 

London,  1912,  Series  B,  CCII,  351. 
Mathewson,  G.  D. :  Lesion  of  the  Branches  of  the  Auriculo-ventricular  Bundle  ; 

Heart,  1912-1913,  IV,  385. 
Oppenheimer,  B.  S.,and  Rothschild,  M.  A. :  Abnormalities  in  the  Q-R-S  Group 

in  the  Electrocardiogram  Associated  with  Myocardial  Involvements  ;  Proc. 

Soc.  Experimental  Med.  and  Biol.,  1916,  XIV,  57. 
Robinson,  G.  C. :    The  Relation  of  Changes  in  the  Form  of  the  Ventricular 

Complex  ...  to  Functional  Changes  in  the   Heart ;   Arch,   of   Internal 

Med.,  1916,  XVII,  830. 
Rothberger,  C.  J.,  and  Winterberg,  H. :  Ueber  die  Beziehungen  der  Herznerven 

zur  Form  des  Elektrokardiogramms :  Arch.  f.  d.  gesammte  Phys.,  1910, 

CXXXV,  506. 
Waller,  A.  D. :   The  Electrical  Action  of  the  Human  Heart ;    Lancet,  May  24, 

1913,  1435. 


CHAPTER  V 

MATHEMATICAL  CONSIDERATIONS  UNDERLYING  THE 
ELECTROCARDIOGRAM 

In  previous  chapters,  the  fact  was  emphasized  that  the  electro- 
cardiographic deviation  represented  the  resultant  of  the  differences  of 
electrical  potential  existing  at  any  given  moment.  The  diagnostic 
significance  of  the  direction  of  the  R  wave  was  also  discussed.  The 
elementary  mathematical  principles,  upon  which  differences  in  the  R 
and  other  deviations  depend,  require  brief  comment. 

Stress  has  been  laid  upon  the  fact  that  the  size  of  the  R  peaks  depends 
upon  the  angle  formed  by  the  "leads"  and  the  "electrical  axis";  the 
nearer  the  electrical  axes  approach  parallelism  to  the  leads,  the  taller 
the  corresponding  peaks ;  the  nearer  these  approach  a  right  angle,  the 
smaller  the  peaks.  The  size  of  the  deviation  thus  varies  with  the  angle 
made  by  the  lead  and  electric  axis.  In  other  words,  the  electrocardio- 
gram is  modified  in  each  lead  by  the  relation  of  the  direction  of  the  current 
to  that  of  the  lead.  Conversely,  the  angles  made  by  these  two  lines 
may  be  computed  from  the  difference  in  size  of  the  deviations  in  the  three 
leads. 

Manifest  Size.  —  Einthoven  has  differentiated  the  actual  size  of  the 
deviations,  as  reproduced  in  the  electrocardiogram,  from  their  "  manifest " 
size  or  the  "  manifest "  difference  of  electric  potential.  He  defines  the 
latter  as  that  dimension  in  millivolts  which  is  derived  when  the  electrical 
axis  and  leads  coincide ;  it  is  the  maximal  size  of  the  electrical  potential 
of  the  heart  in  that  lead.  The  manifest  size  of  any  deviation  is  com- 
puted from  the  registered  actual  electrocardiogram.  Einthoven  and  his 
pupils,  Fahr  and  de  Waart,  have  laid  down  mathematical  principles  by 
which  it  is  possible  to  estimate  the  angles  formed  by  the  electrical  axes 
with  the  leads.  If,  for  purposes  of  simplification,  the  lines  of  the  three 
leads  be  conceived  as  forming  the  sides  of  an  equilateral  triangle  (Fig.  70, 
R,  L,  F)  and  its  middle  point,  II,  represent  the  heart,  the  size  of  the  R 
deviations  in  the  three  leads  is  obtained  by  the  right-angled  projection 
of  the  deviations  upon  the  electrical  axis  passing  through  the  point  H. 

39 


/ 


40 


CLINICAL  CARDIOLOGY 


From  these,  data  are  derived  for  the  determination  of  the  angle  formed 
by  the  electrical  axis  and  the  leads.1 

Measurement  of  the  Angles  Made  by  the  Leads  and  the  Electrical 
Axis.  —  If  smaller  angles  be  discarded  and,  for  purposes  of  clinical  ap- 
proximation, only  those  considered  which  are  multiples  of  30°,  the  com- 
putation of  E1:E2:E3  (Fig.  70)  is 
much  simplified ;  for  example, 

When 

a=    0°,then£l:£2:£3  =  l:  +  .5:-.5 

a  =  30°,  then  £1:£2:£3  =  1:1:0 

a  =  60°,then£l:£2:£3=+.5:l:-.5 

a  =  90°,  then  E  1:E2:E3=0:  1:1 

etc. 

From  these  numerical  proportions, 
the  angle  a  can  be  approximated  within 
30°.  The  "  manifest "  equals  the  actual 
size  of  R  1  (E  1,  Fig.  70)  when  a  equals 
0°;  of  R2  (E2)  when  a  equals  60°,  and 
of  R  3  (E  3)  when  it  equals  120°.  For 
the  exact  determination  of  this  angle, 
tables  are  required.  In  the  Appendix  to 
this  chapter  (q.v.)  there  is  one  table  for 
approximation  within  10°  ;  by  the  use  of 
the  second  table  (Interpolation  Table) 
the  exact  angle  may  be  computed.  For 
example,  if  R  1  equals  3.2,  R  2  equals 
12.5,  and  R  3  equals  9.3,  then  E1(R1): 
E  2  (R  2)  :  E  3  (R  3)  =  3.2  :  12.5  :  9.3. 
To  derive  an  approximation  within  10° 
(Table  I),   12.5,   the    tallest    deviation, 

becomes   the  denominator,    thus:  • 

12.5 

Substituting  this  fraction  for  12.5  in  the 

equation,  we  find  E  1 :  E  2  :  E  3  =  2.6  : 

10 :  7.4.      Furthermore,    from  the   same 

table   we   note  these  figures  determine 

that  the  angle  a  falls  between  70°  and 

80° :  and  that  E  1  between  70°  and  80° 


Fig.  70.  —  (From  Einthoven,  Fahr, 
and  De  Waart — "Ueber  die 
Richtung  und  Manifest  Groesse 
der  Potentialschwankungen, "  etc. 
Archive  f.  d.  ges.  Physiologie,  1913, 
CL,  308) .  The  right  and  left  arms 
and  left  foot  (designated  R,  L,  F, 
respectively)  form  the  angles  of 
an  equilateral  triangle.  The  point 
H  is  in  the  center  and  represents 
the  heart.  If  the  arrow  EA  rep- 
resent any  given  electrical  axis, 
the  angle  it  forms  with  the  first 
lead  (RL)  he  represented  by  ci, 
and  any  given  length  pq  be  called 
E,  the  right  angle  projection  of 
its  length  will  give  its  correspond- 
ing value  in  the  various  leads ; 
that  is,  in  L  I  it  will  equal  E  1  ; 
and  L  II,  E2  and  in  L  III,  E  3. 
The  distances  El,  E 2,  EZ  are 
proportional,  that  is,  E 1  :E2:E3. 
Since  any  angle  of  an  equilateral 
triangle  is  equal  to  60°,  the  follow- 
ing trigonometrical  formulae  are 
derived : 

E  1  =  E  cos  a  ; 

E  2  =  E  cos  «  -  60°  ; 

E3  =  E  cos  (120-  a); 

Tp  o  E1  O  p  1 

The  formula   E  3  =  E  2  -  E 1   is  of 

special  importance,  for,  given  the 
heights  of  deviations  in  any  two 
leads,  the  height  of  the  remaining 
peak  may  be  derived. 


1  (See  also  legend  with  Fig.  70.)  To  insure  mathematical  accuracy  it  is  neces- 
sary to  measure  the  R  deviations  at  identical  phases  of  the  heart  cycle.  With 
this  in  view,  two  galvanometers  may  be  simultaneously  employed  ;  one  to  record 
sound  records,  the  other  to  record  the  electrocardiograms.  The  position  of  the 
Q,  R  and  S  in  identical  cardiac  phases  is  thus  determined.  Although  this  method 
is  necessary  for  absolute  accuracy,  unless  phasic  differences  of  the  heart  cycle 
produce  marked  changes  in  the  electrocardiogram,  measurements  derived  from 
the  ordinary  electrocardiogram  are  sufficiently  exact  for  clinical  purposes. 


MATHEMATICAL  CONSIDERATIONS 


41 


has  a  value  between  3.5  and  1.8,  a  difference  of  2.7.  In  Table  II 
(Interpolation  Table,  Third  Column)  the  nearest  approximation  to  this 
difference  is  2.6,  which  is  equivalent  to  6° ;  hence,  a  =  70°  +  6°  =  76°. 

As  another  example,  suppose  T  1  =  4,  T  2  =  1.5,  and  T  3  =  —  3.5, 
we  then  have  the  proportion  E  1:  E  2:  E  Z  =4:1. 5:  —  2.5.  To 
derive  approximation  within  10°  we  multiply  by  the  fraction  Y",  4  being 
the  tallest  deviation.  Then  E1:E2:E3  =  10 :  3.75  :  -  6.25.  From 
Table  I,  this  proportion  shows  that  the  angle  a  is  between  0°  and  —  10°, 
and  also  that  E  2  varies  from  5  to  3.5.  In  Table  II,  its  nearest  approxi- 
mation is  3.8,  an  angle  of  8°.     Hence,  a  =  0°  —  8°  =  —  8°. 

Since  the  value  of  the  angle  alpha  can  be  computed,  it  is  possible 
by  trigonometry  1  to  determine  the  manifest  size  (Fig.  70)  of  the  various 
deviations. 

In  a  schematic  diagram  by  Pardee  (Fig.  71),  based  upon  the  Ein- 
thoven  conception  of  the  leads  forming  a  triangle  with  the  heart  in  the 


Fig.  71.  —  (From  H.  E.  Pardee — "Form  of  the  Electrocardiogram,"  Journal  of  the 
American  Medical  Association,  1914,  LXII,  1311).  a,  b,  c,  represent  the  numerical 
value  of  the  deflection  caused  by  an  action  current  in  leads  /,  II,  III,  respectively. 
b  =  a+  c  and  will  be  directed  upwards  or  downwards  according  as  a  and  c  are  directed  ; 
+  before  the  letter  signifies  an  upward  deflection ;   —  signifies  a  downward  deflection. 

center,  the  angle  a  can  be  roughly  measured  by  conceiving  the  direction 
of  the  electrocardiographic  current  as  lying  in  one  of  6  sectors  of  60° 
each.  Thus,  currents  or  electrical  axes  between  +  30°  and  +  90° 
(the  normal  segment)  give  +  R  I  +  R  2  +  R  3. 


1  The  f onnulse  by  which  the  value  of  E  (the  manifest  size)  may  be  derived  are 

7*         El 


COS  a. 

E 

E2 

cos(a  —  60°) 

E 

ES 

cos  (120°  -a) 

42  CLINICAL   CARDIOLOGY 

Axes  between  +  90°  and  +  150°  give  -  Rl  +  R2  +  R3 
Axes  between  +  150°  and  -  150°  give  -R1-R2+R3 
Axes  between  -  150°  and  -  90°  give  -R1-R2-RZ 
Axes  between  -  90°  and  -  30°  give  +  Rl  -  R2  -  R  3 
Axes  between  -  30°  and  +  30°  give  +  Rl  +  R2  -  R3 
These  results  are  diagramrnatically  shown  in  Fig.  72. 
By  these  computations  and  methods,  accurate  knowledge  of  the 
direction  and  size  of  the  electrical  axis  and  of  the  electrical  balance  of 
the  heart  is  obtained,  but  definite  information  regarding  the  origin  of 
the  excitation  wave  is  not  thus  derived.     A  knowledge  of  the  manifest 
size  in  conjunction  with  the  electrical  axis  helps  to  diagnose  the  most 


SL'aSst.Isl. 


Kt5'A 


Fig.  72.  —  Diagram  showing  the  direction  of  the  leads  with  currents  (electrical  axes)  at 
various  angles.  The  circle  is  divided  into  six  sectors  of  60°  each.  The  direction  of  the 
currents  is  marked  bv  the  arrow  heads,  the  ventricular  deviations  for  the  respective 
leads  by  22  1,  22  2,  22  3. 

likely  point  or  points  of  origin  of  the  excitation  wave.  By  further  am- 
plification and  applications  of  the  Einthoven  formulae,  Fahr  and  Weber 
have  concluded  as  follows :  The  deviation  Q  results  from  excitation  in 
the  neighborhood  of  the  middle  zone  of  the  heart :  the  papillary  muscles 
and  their  environment.  The  apex  of  R  is  the  resultant  of  excitation  in 
the  base  of  the  heart,  usually  over  its  middle  portion.  This  area. is 
ordinarily  to  the  left,  but  sometimes  to  the  right  of  the  middle  line. 
The  deviation  S  in  general  denotes  apical  negativity ;  the  electrical  center 
is  usually  to  the  left,  but  may  be  to  the  right  of  the  median  line.  The 
deviation  T  is  the  end  of  the  excitation  wave.  As  a  rule,  it  results  from 
excitation  of  the  ventricular  base,  to  the  right  or  left  of  the  median 
line. 

It  is  thus  apparent  that  the  electrical  excitation  wave  in  the  ventricle 
normally  proceeds  in  the  following  sequence :  the  neighborhood  of  the 
papillary  muscles,  the  base  of  the  heart,  the  apical  portion,  and  finally 
the  basal  area. 


MATHEMATICAL   CONSIDERATIONS 


43 


APPENDIX  i 


Chapter  V 


Table  I 


Table  II 


X 

-  -  i 

Interpolation  Table 

Registered  Potential 

Differences 

e 

&  S3  2 

z  Z  r 

a 

Differences 
in  Degrees 

Potential 
Differences 

+  e 

Differences 

in  Degrees 

E 

e1 

e2 

E 

0° 

0 

10° 

11.5 

u° 

10 

5,0 

-5,0 

10,0 

f?: 

i  4 

0,4 
0.8 

8° 

6° 

11.3 

10° 

10 

6,5 

-  3,5 

10.2 

11.1 

20° 

10 

8,2 

-  1,8 

10,7 

i6 

l  8= 

1,2 

4° 

11.0 

30° 

10 
8,2 
6,5 
5,0 

10 

10 
10 
10 

0 

1,8 
3,5 
5,0 

11.5 
10,7 
10.2 
10.0 

1,5 

2° 

10.% 

40° 
50° 
60° 

10- 

1,8 

0° 

10.7 

f  2° 

2.2 

8° 

10. 5 

70° 

3,5 

10 

6,5 

10,2 

nk 

2,5 

6° 

10.4 

80° 

1,8 

10 

8.2 

10,7 

2,9 

4° 

:    \ 

i 

I  8° 

3  2 

10  2 

90° 

0 

10 

10 

11,5 

100° 

-  1,8 

-  3,5 

8,2 
6,5 

10 
10 

10,7 
10,2 

10° 

3,5 

0° 

10.2 

110° 

[2° 

3.8 

8° 

10.1 

120° 

-  5,0 

5,0 

10 

10.0 

in  £ 

4,1 

6° 

10.1 

130° 

-  6,5 

3,5 

10 

10.2 

4,4 

4° 

10.0 

140° 

-  8,2 
-  10 
10 

1,8 
0 

-  1,8 

-  3,5 

10 
10 

8,2 

6.5 

10.7 
11,5 
10  7 

[8° 

4,7 

2° 

10.0 

150° 
160° 

10 

5,0 

0° 

10,0 

170° 

-  10 

10,2 

+180° 

-10 

-5,0 

5,0 

10,0 

-  170° 

-  10 

-  6,5 

3,5 

10.2 

-  160° 

-  10 

-  8,2 

1,8 

10,7 

-  150° 

-  10 

-  10 

0 

11.5 

-  140° 

-  8,2 

-  10 

-  1,8 

10.7 

-130° 

-6,5 

-  10 

-  3,5 

10.2 

-  120° 

-5,0 

-  10 

-  5,0 

10.0 

-  110° 

-  3,5 

-  10 

-  6,5 

10.2 

-  100° 

-  1,8 

-  10 

-  8,2 

10,7 

-90° 

0 

-10 

-10 

11,5 

-80° 

1.8 

-  8,2 

-10 

10.7 

-70° 

3.5 

-  6,5 

-  10 

10.2 

-60° 

5.0 

-  5.0 

-  10 

10.0 

-50° 

6.5 

-  3.5 

-  10 

10.2 

-40° 

8,2 

-  1.8 

-  10 

10.7 

-30° 

10 

0 

-  10 

11.5 

-20° 

10 

1.8 

-  8.2 

10.7 

-10° 

10 

3.5 

-  6.5 

10.2 

0° 

10 

5.0 

-5.0 

10.0 

1  These  tables  and  the  examples  in  the  text  were  taken  from  Einthoven.  Fahr 
and  de  TTaart  "Ueber  die  Riehtungen  und  die  Manifest  Grosse  der  Potential- 
sehwankungen,  ....  des  Elektrokardiogramms.'!  (Arch.  f.  d.  ges.  Phvsiologie, 
913,  ef.  p.  275.) 


CHAPTER  VI 
COURSE   OF  THE  EXCITATION  WAVE 

By  means  of  careful  experimental  investigations  based  upon  meas- 
urements of  electrocardiograms  led  off  from  different  parts  of  the 
cardiac  surface,  Lewis  clearly  demonstrated  that  the  excitation  wave  in 
the  auricle  spreads,  ripple-like,  from  the  sino-auricular  node  as  a  center ; 
it  follows  the  chief  auricular  muscle  bands  which  radiate  from  this 
region,  and  spreads  thus  throughout  the  auricular  tissue  and  septum  to 
reach  the  A-V  bundle.  "The  excitation  wave  appears  in  some  parts  of  the 
right  auricle  before  some  portions  of  the  left,  and  vice-versa  "  (Lewis). 

The  spread  of  the  ventricular  excitation  wave  does  not  follow  the 
anatomical  arrangement  of  the  musculature.  After  reaching  the  A-V 
node,  it  begins  almost  simultaneously  in  different  parts  of  an  area 
supplied  most  directly  by  the  right  branch  of  the  A-V  bundle ;  this  is 
the  part  of  the  right  ventricular  wall  which  overlies  the  large  anterior 
papillary  muscle ;  later,  the  remainder  of  the  right  ventricle  becomes 
active.  In  the  left  ventricle  the  wave  also  follows  a  definite  course. 
The  earliest  point  to  be  excited  is  the  vortex  of  the  left  ventricle  or 
the  extreme  apex ;  about  Tm  second  later  the  neighboring  points  are 
activated ;  excitation  of  the  remainder  of  the  left  ventricle  is  almost 
simultaneous.  The  cardiac  base  is  usually  last  affected,  and  its  activity 
is  practically  coincident  with  activity  in  the  conus  region.  Since  some 
ventricular  areas  are  excited  simultaneously,  the  ventricular  wall  must 
be  reached  by  simultaneous  impulses  traveling  along  a  large  number  of 
paths ;  by  experiments,  these  have  been  shown  to  be  the  Purkinje  fibers. 
But  some  parts  of  the  ventricular  musculature  not  supplied  by  free, 
branching  Purkinje  strands  (e.g.  the  conus  region  beneath  the  pul- 
monary valves)  are  activated  very  early.  This  is  accounted  for  by  the 
thinness  of  the  ventricular  musculature  in  the  region  of  the  right  papil- 
lary muscle.  The  varying  thickness  of  the  musculature  also  accounts 
for  excitation  reaching  the  thinnest  area  first  and  later  the  thicker  left 
ventricular  vortex.  Excitation  is  found  to  travel  extremely  rapidly 
through  the  conduction  system.  In  brief,  then,  the  excitation  wave 
appears  almost  simultaneously  along  the  interior  of  both  ventricles. 
The  activation  of  the  ventricular  surface  is  only  partly  dependent  upon 

44 


COURSE   OF  THE   EXCITATION   WAVE  45 

its  distance  from  the  Purkin je  fibers ;  it  is  mainly  controlled  by  the  muscle 
thickness  overlying  the  latter,  for  the  excitation  wave  is  conceived  as 
appearing  on  the  surface  by  directly  piercing  the  musculature.  Thus, 
by  a  different  method,  a  result  similar  to  that  of  Fahr  and  Weber  has  been 
reached  regarding  the  course  of  the  ventricular  excitation  wave. 

(4)  Variations  of  the  T  Wave 
(See  Classification,  Chapter  V.) 

The  T  deviation  is  normally  monophasic  and  directed  positively 
(i.e.  upwards)  in  the  three  leads  (Fig.  37),  its  height  varying  between  2 
and  3  millivolts.  It  is  occasionally  quite  tall  (Fig.  73,  Plate  VIII)  and 
sometimes  exceeds  in  height  the  corresponding  ventricular  spike  (Fig.  74, 
Plate  VIII).  Not  infrequently,  it  is  deviated  downwards  in  the  third 
lead  (Fig.  75,  Plate  VIII).  The  clinical  conditions  in  which  the  T  wave 
is  diphasic  or  deviated  downwards  in  the  first  or  second  leads  are  only 
imperfectly  understood ;  hence,  inferences  drawn  therefrom  are  for  the 
present  only  tentative. 

A  positively  deviated  T  denotes  that  the  excitation  wave  has  entered 
the  ventricular  base  (Chapter  V) .  In  a  number  of  cases  of  heart  disease, 
especially  of  the  myocardium,  T  I,  T II,  or  both,  may  be  small  or  nega- 
tive (Fig.  56,  Plate  VII ;  Fig.  76,  Plate  IX),  indications  of  an  abnormal 
termination  of  the  excitation  wave  in  the  ventricle.  Much  diagnostic 
significance  has  been  given  to  these  negative  T  deviations,  especially 
since  Einthoven  regarded  a  well-marked  positive  T  as  a  sign  of  good 
cardiac  contractility,  and  its  absence,  or  diminution,  the  reverse.  It  is, 
however,  now  known  that  the  T  wave  may  be  absent  in  normal,  and  be 
very  well  marked  and  positive  in  diseased,  hearts. 

Effect  of  Digitalis  on  the  T  Wave.  —  It  has  recently  been  demon- 
strated that  digitalization  of  a  patient  with  heart  disease  may  convert 
a  positive  T  to  a  flattened  or  negative  wave.  Though  this  may  be  partly 
due  to  muscular  ventricular  redistribution  as  the  result  of  relief  of  decom- 
pensation, the  chief  factor  is  probably  alteration  in  the  contractility  of 
the  heart  muscle.  Pharmacological  experiments  in  frogs  and  mammals 
have  shown  that  digitalis  produces  diminished  diastolic  relaxation  of  the 
apical  region.  In  the  toxic  stage  there  is  systolic  standstill  of  the  apex, 
while  the  base  relaxes  in  diastole.  It  is  possible,  therefore,  that  similar 
influences  affect  the  digitalized  human  heart,  producing  continued 
apical  activity  and  thus  a  negatively  deviated  T  wave.  The  usual 
effect  of  digitalis  administration  on  the  T  wave  may  not  become  evident 
until  atropine  has  been  injected.  Atropine  apparently  unmasks  and 
removes  the  inhibitory  effect  of  the  drug ;  thereafter  the  full  influence 
of  digitalis  on  the  heart  can  be  observed.  Some  years  ago,  Einthoven 
made  the  observation  in  one  case  that  as  the  result  of  exercise,  a  nega- 
tively deviated  T  III  in  a  normal  heart  became  positive.  It  has  also 
been  recently  demonstrated  in  a  few  cases  that  a  negative  T  in  decom~ 


46  CLINICAL  CARDIOLOGY 

pensated  hearts  may  become  positive  with  restoration  of  compensation. 
The  change  is  probably  the  result  of  nerve  influence  occurring  during 
exercise.  This  view  is  based  upon  the  fact  that  exercise  is  accompanied 
by  accelerator  excitation,  and  that  various  experimental  observations 
have  shown  a  definite  correlation  between  accelerator  stimulation 
and  the  size  of  the  T  wave.  It  therefore  seems  probable  that  a  positive 
T  produced  by  exercise,  or  by  the  restoration  of  compensation,  is  due 
to  a  neurogenic  influence  acting  upon  the  ventricular  base.  Whether, 
under  these  conditions,  a  positive  T  is  to  be  regarded  as  a  favorable 
change  is  an  open  question  and  awaits  further  corroboration.  Hence, 
clinical  inference  respecting  its  value  should  for  the  present  be  guarded. 

REFERENCES 

Chapters  V  and  VI 

Barringer,  T.  B.,  Jr.,  and  Teschner,  J. :  The  Treatment  of  Cardiac  Insuffi- 
ciency by  a  New  Method  of  Exercise.with  Dumb-bells  and  Bars  ;  Archives 
of  Internal  Medicine,  1915,  XVI,  795. 

Cohn,  A.  E.,  Fraser,  F.  R.,  and  Jamieson,  R.  A. :  The  Influence  of  Digitalis  on 
the  T  wave  of  the  Human  Electrocardiogram;  Journal  of  Experimental 
Medicine,  1915,  XXI,  593. 

Cushny,  A.  R. :  Pharmacology  and  Therapeutics,  Ed.  1913. 

Einthoven,  W. :  Weiteres  ueber  das  Elektrokardiogram ;  Pflueger's  Archiv, 
1908,  CXXII,  536. 

Einthoven,  W. :  Ueber  die  Deutung  des  Elektrokardiogramms ;  Archiv  fuer 
die  ges.  Phvsiologie,  1912,  CXLIX,  65. 

Einthoven,  W.,  Fahr,  G.,  and  de  Waart,  A. :  Ueber  die  Richtung  und  Manifest 
Groesse  der  Potentialschwankungen  .  .  .  des  Elektrokardiogramms ;  Archiv 
fuer  die  ges.  Physiologie,  1913,  CL,  275. 

Fahr,  G. :  On  Simultaneous  Records  of  the  Heart  Sounds  and  the  Electro- 
cardiogram; Heart,  1912,  IV,  147. 

Fahr,  G.,  and  Weber  :  Ueber  die  Ort  und  Bestimmungen  der  Erregung  .  .  •  mit 
Hilfe  der  Elektrokardiographie ;  Deutsches  Archiv  fuer  klinische  Medizin, 
1914-15,  CXVII,  361. 

Lewis,  T. :   Lectures  on  the  Heart,  3. 

Neuhof,  S. :  Digitalis  Therapy  ;  New  York  Medical  Journal,  1915,  CI,  241. 

Pardee,  H.  E.  B. :  Form  of  the  Electrocardiogram;  Journal  of  the  American 
Medical  Association,  1914,  LXII.  1311. 

Rothberger,  C.  J.,  and  Winterberg,  H. :  Ueber  die  Beziehungen  der  Herznerfen 
zur  Form  des  Elektrokardiogramms  ;  Archiv  fuer  die  ges.  Physiologie,  1910, 
CXXXV,  506. 

Waller,  A.  D. :   Electrical  Action  of  the  Human  Heart ;   Lancet,  May  24,  1913. 


CHAPTER  VII 

THE  ARRHYTHMIAS  —  THEIR  POLYGRAPHIC,  ELECTROCAR- 
DIOGRAPHIC  AND   CLINICAL  RECOGNITION 

The  passage  of  the  normal  impulse,  as  exemplified  in  polygraphic  and 
electrocardiographic  tracings  of  the  normal  rhythmic  cardiac  mechanism, 
has  already  been  described.  We  shall  now  treat  of  those  abnormal 
mechanisms  known  as  cardiac  arrhythmias  and  irregularities.  A.  E.  Cohn 
has  succinctly  grouped  the  arrhythmias  as  coming  under  variations  of 
a  few  fundamental  normal  functions.  He  states  that  cardiac  irregulari- 
ties arise  from  the  abnormal  passage  of  the  impulse,  from  abnormal 
sequence  of  contraction  of  the  pairs  of  chambers,  and  from  abnormal 
coordination  of  the  muscle  mass.  So  far  as  possible,  these  basic  consider- 
ations have  been  incorporated  into  my  Tabulation  of  the  Arrhythmias. 
As  will  be  seen,  I  have  grouped  almost  all  the  arrhythmias  as  due  to  those 
arising  in  the  auricle,  those  arising  in  the  ventricle,  and  those  arising 
in  the  specialized  tissues,  the  sino-auricular  and  the  auriculo-ventricular 
nodes. 


TABULATION  OF  TYPES  OF  ARRHYTHMIAS  AND  CARDIAC 
IRREGULARITIES 


Auricular 
Arrhythmias  ' 


II. 


III. 


f  from  the  normal  site. 
Auricular  Extrasystoles  <  from  an  abnormal  site  (ec- 

[     topic). 
Paroxysmal  Tachycardia  of  Auricular  Origin. 

f  (1)  Auricular  Fibrillation. 

Auricular  Ineoordina-     <§>  tScUnSnlntcnne. 

diate  between  Flutter 
and  Fibrillation. 


A'.   Nodal  Extrasystoles. 


B. 


Ventric- 
ular 

Arrhyth- 
mias 


I.  Ventricular  Extrasystoles  (from  Right  or  Left  Ventricle) . 
II.   Interpolated  Extrasystoles. 

III.  Automatic  Ventricular  Activity-Ventricular  Escape. 

IV.  Paroxysmal  Tachycardia  of  Ventricular  Origin. 

V.  Ventricular  Iucoordinati„n{  g>  ^SStLSeS^ 


C.   True  Bradycardia. 


47 


48 


CLINICAL  CARDIOLOGY 


f  I. 


D. 


Arrhythmias 
Produced 
by    Abnor- 
mal   Se- 
quence   of  { 
Contrac- 
tion op  Au- 
ricles    AND 
Ventricles 


II. 


Disturbance  in 
the      Sino- 
aurieular 
Node 


Disturbance  in 
Atrioven- 
tricular 
Node 


(1)  Sinus  Arrhythmia  or  Irregularity. 

(2)  Sino-auricular    Block     (Sinus 

Block). 

(3)  Blocked  Auricular  Beat. 

(1)  Prolonged  Conduction  Time. 

(2)  Shortened  Conduction  Time. 

(3)  Backward  Conduction. 
(a)  Incomplete 


(4) 


Auriculo- 
ventric- 
ular  Heart 
Block 


(&) 


Heart 
Block. 
Complete 
Heart 
Block 
(Dissocia- 
tion). 


It  is  the  aim  of  graphic  methods  to  exactly  transcribe  the  cardiac 
mechanisms,  normal  and  abnormal.  It  has  always  been  the  aim  of 
progressive  clinical  medicine  to  adopt  and  adapt  the  knowledge  gained 
by  the  use  of  exact  instrumental  methods  for  immediate  use  at  the  bed- 
side, where  instruments  may  not  be  available.  It  is  thus  that,  in  the 
light  of  knowledge  gained  by  a  careful  study  of  the  graphic  methods, 
and  with  a  full  appreciation  of  the  physiological  pathology  involved,  it  is 
possible  to  diagnose  most  types  of  arrhythmia  by  ordinary  methods  of 
examination.  For  this  purpose,  the  stethoscope  should  be  placed  over 
the  cardiac  apex  and  the  fingers  kept  on  the  pulse ;  the  neck  should  be 
carefully  scrutinized  for  jugular  and  carotid  pulsations  (a  and  c  waves). 
The  value  of  keen  observation  will  be  discussed  in  connection  with  the 
clinical  recognition  of  the  arrhythmias. 


A   I.     Auricular  Extrasystoles 

Some  preliminary  observations  regarding  the  general  nature  of 
extrasystoles  —  auricular,  ventricular,  and  nodal  —  are  required  before 
their  various  types  and  instrumental  and  clinical  recognition  are  dis- 
cussed. 

Contractions  of  auricle  or  ventricle  which  anticipate  the  normal 
rhythmic  time  of  their  occurrence  and  disturb  the  normal  rhythm  are 
known  as  extrasystoles  or  premature  contractions.  Fundamentally, 
the  normal  passage  of  the  impulse  is  disturbed.  Extrasystoles  were 
formerly  termed  '  pulsus  bigeminus.'  The  term  'premature  contraction' 
is  preferable  because  it  so  aptly  describes  the  phenomenon.  Extra- 
systole  is  in  a  sense  a  misnomer,  for  the  contraction  is  not  '  extra  '  or 
additional ;  it  is  simply  anticipatory.  However,  since  '  extrasystole '  is 
commonly  used,  it  will  be  here  employed.  If  extrasystoles  recur  at 
regular  intervals  after  each  normal  beat,  the  resultant  rhythm  is  known 
as  coupling,  coupled  rhythm,  or  coupled  beats. 

There  are  certain  characteristics,  as  Lewis  has  pointed  out,  which 
differentiate  the  premature  from  the  normal  contraction.  The  physio- 
logical or  homogenetic  beat  is  one  of  a  series  of  similar  rhythmic  contract 


THE   ARRHYTHMIAS 


49 


tions ;  the  contractions  are  equally  spaced  ;  there  is  an  orderly  building 
up  of  impulse  formation  which  requires  at  least  one  half  second  for  each 
beat.  This  power  of  rhythmic  impulse  formation  resides  chiefly,  if  not 
entirely,  in  the  specialized  tissues  of  the  sino-auricular  node,  of  the 
atrio-ventricular  node,  or  in  the  bundle  of  His  (Fig.  77).  Regarding  the 
premature,  extrasystolic,  heterogenetic,  or  pathological  contraction, 
whether  single  or  multiple,  there  is  an  exceedingly  rapid,  abrupt,  or  no 
impulse  formation.  Ventricular  extrasystoles,  for  example,  may  follow 
each  other  at  intervals  as  short  as  .25  second  or  less.  Extrasystoles 
are  further  differentiated  from  normal  beats  by  their  prematurity  and  by 
their  lack  of  rhythmic  tendency ;   even  when  multiple  or  occurring  in 


Fig.  77. 


Fig.  78. 


Fig.  79. 


Fig.  SO. 


Fig.  81. 


Fig.  82. 

Figs.  77-82.  —  Diagrams  showing  the  origin  of  physiological  and  pathological  contractions. 
Figs.  77-78.  —  S-A  =  sino-auricular  node  ; 

A-V  =  part  of  the  atrio-ventricular  conduction  system. 
Fig.  77.  — XX  shows  the  origin  of  homogenetic  beat  in  the  sinus  region  with  normal 

propagation  in  the  junctional  tissue. 
Fig.  78.  —  X  =  ventricular  extrasystole  —  heterogeneous  ectopic  beat. 
Fig.  79.  — X  =  auricular  extrasystole  — -  heterogeneous  ectopic  beat. 
Fig.  80.  — X  =  nodal  extrasystole. 

Fig.  81  shows  the  disturbance  in  rhythm  with  a  premature  auricular  contraction. 
Fig.  82  shows  the  disturbance  in  rhythm  with  a  premature  ventricular  contraction. 


50 


CLINICAL  CARDIOLOGY 


showers,  the  rate  of  production  is  usually  maximal.  There  is  no  relation 
between  the  heightened  activity  of  the  physiological  heart  rhythm  and  the 
prevalence  of  extrasystoles.  Often,  influences  which  depress  the  one 
favor  the  occurrence  of  the  other ;  such  an  example  is  chloride  of  potas- 
sium in  the  experimental  animal.    Premature  contractions  bear  a  different 


Fig.  S3.1         R  =  rhythmic  beat ;  C.P  =  compensatory  pause ; 

r'  =  extrasystole ;  R'  =  larger  post  extrasystolic  beat. 

In  the  jugular  tracing,  the  premature  wave  c'  is  synchronous  with  r'.  Its  foot-point  is 
determined  by  measuring  off  with  dividers  the  distance  Rr'  from  the  preceding  rhythmic 
c(Rr'=  cc').  The  auricular  beat  A  is  not  premature.  It  falls  at  its  rhythmic  time ; 
hence,  the  inter-auricular  distance  a- A'  is  equal  to  the  normal  beat  (R).  A  occurs  be- 
fore the  c'  wave  has  completed  its  fall,  hence  the  abnormal  width  of  the  combined  c'A. 
The  A  wave  is  often  not  indicated  as  a  distinct  part  of  the  c'A  because  it  may  be  lost  in 
the  more  prominent  c'  wave. 

relation  to  the  cardiac  nerves  than  the  normal  beats;  for  instance, 
gradually  increased  right  vagus  stimulation  retards  the  normal  rhythm ; 
it  has  no  effect  on,  or  produces  abrupt  cessation  in,  a  series  of  premature 
contractions.     It  can  be  electrocardiographically  shown  that  the  latter 


Fig.  85. 
Figs.  84,  85.  —  Ventricular  extrasystoles  with  typical  compensatory  pauses. 

rarely  originate  from  the  normal  rhythmic  center.  Finally,  the  nearer 
the  physiological  beat  originates  in,  and  approaches  the  vicinity  of, 
the  superior  vena  cava,  the  faster  the  rhythm.  This  law  does  not 
apply  to  extrasystoles ;  their  rate  does  not  depend  upon  their  origin 
in  auricle  or  ventricle. 

Premature  beats  (Figs.  78-82),  because  of  their  inherent  weakness 
or  because  the  wave  is  not  properly  directed  against  the  aortal  cusps, 

1  In  all  the  polygraphic  tracings,  the  time-marker  measures  \  second. 


THE  ARRHYTHMIAS 


51 


are  occasionally  '  frustrane '  or  '  abortive ' ;  that  is,  they  either  do  not 
open  the  aortal  cusps  or  do  so  too  slightly  to  produce  a  palpable  radial 
wave.  These  frustrane  contractions  are  sometimes  termed  '  missed 
beats,'  an  evident  misnomer,  because  ventricular  contractions  do  actually 
occur,  but  the  blood  is  not  propagated  as  a  pulse  wave.  Not  only  may 
abortive  contractions  escape  palpation,  they  may  even  be  too  minute 
to  be  seen  in  radial  tracings.  In  such  instances  the  phlebogram  shows 
the  usual  evidence  of  premature  contractions  (Figs.  86,  c' ,  87c') ;  the 
method  of  seeking  the  point  of  incidence  of  the  rhythmic  auricular 
beat  has  already  been  shown  {A  wave,  Figs.  83,  84,  85). 


Fig.  86. 


Figs.  86,  87.  —  Ventricular  extrasystoles  with  c'  in  the  jugular  but  no  representation  in 
the  radial  tracing.  X  marks  the  point  where  the  extrasystole  should  have  produced 
a  pulse  wave. 


Heterogenetic  beats,  single  or  multiple,  that  originate  outside  of  the 
sinus  region  have  been  called  "  ectopic  "  contractions  (Lewis) .  Auricular 
extrasystoles  are  usually  ectopic,  but  this  can  only  be  demonstrated 
electrocardiographically  by  the  difference  in  the  form  of  the  abnormal 
auricular  complex  (P  waves,  Chapter  IV).  "Ectopic"  auricular  con- 
tractions, that  is,  those  arising  from  an  abnormal  site,  are  not  neces- 
sarily premature  in  their  occurrence  and  hence  may  not  disturb  the 
normal  rhythm. 

When  auricular  extrasystoles  are  present,  the  ventricle  usually  re- 
sponds to  the  premature  auricular  contraction  after  normal  conduction 
time. 

As  may  be  seen  in  the  polygram,  auricular  extrasystoles  produce 
radial  waves  of  varying  size  and  strength  (/•',  Figs.  88,  89) ;  frustrane  con- 
tractions are  comparatively  rare.  The  auricular  extrasystole  in  the 
jugular  tracing  is  usually  marked  by  normal  conduction  time  between  it 
and  the  answering  beat  (a',  c' ',  Figs.  88-89) ;  the  conduction  time,  how- 


52 


CLINICAL   CARDIOLOGY 


ever,  is  occasionally  diminished  («',  Figs.  90-91),  or  that  of  the  succeed- 
ing beat,  increased  (Fig.  92  a).     Extrasy stoles  are  sometimes  multiple 


Figs.  88,  89.  — -  Auricular  extr asystoles.    The  auricular  beat  a'  is  premature  and  is  followed 
by  the  c  wave.     The  v  wave  of  the  rhythmic  beat  has  fallen  with  a'. 


(Figs.  93-94).  If  the  first  one  is  registered  in  the  radial  curve,  the  latter 
resembles  coupled  rhythm ;  the  jugular  tracing  will  then  reveal  the 
frustrane  extrasystoles  (Figs.  93,  a",  c" ,  94,  a",  c" ,  a"',  c'"). 

As  seen  in  the  electrocardiogram,  when  auricular  extrasystoles 
originate  in  the  pacemaking  area,  i.e.  in  the  normal  site,  the  complexes 
are  identical  in  shape  with  those  of  the  normal ;  the  only  distinguishing 
feature  is  their  prematurity.  The  ventricle  usually  responds  after  a 
normal  P-R  interval,  and  its  complex  is  the  same  as  the  other  rhythmic 
beats  because  it  follows  the  normal  path  in  the  conduction  system 
(Figs.  95,  96,  97,  Plate  IX).  The  premature  auricular  contraction  often 
falls  at  a  time  when  its  complex  is  superimposed  upon  the  T  wave 
(Fig.  98,  Plate  IX),  so  that  upon  superficial  examination  the  P  wave 
appears  absent.  Careful  scrutiny,  however,  indicates  that  the  com- 
posite P-  T  wave  is  somewhat  taller  and  thicker  than  the  P  wave  alone 
(Fig.  97,  Plate  IX).  Ectopic  auricular  contractions  which  originate  in  an 
abnormal  site  outside  the  sinus  area  show  their  origin  by  change  of  com- 
plex. This  is  well  exemplified  in  Fig.  99  (Plate  X),  which  demon- 
strates beats  starting  from  different  ectopic  foci  {A,  Ex.  1 ;  A,  Ex.  2) ; 
the  abnormal  complexes  are  deviated  upwards  and  resemble  the  normal. 
This  probably  indicates  an  origin  close  to  the  pacemaker.  It  is  to  be 
noted  that  the  ectopic  beats  are  neither  premature  nor  are  they  followed 
by  compensatory  pauses ;  the  only  feature  differentiating  them  from  the 
normal  is  their  difference  in  form. 

Clinical  Recognition  of  Extrasystoles  (Premature  Contractions).  — 
Isolated  extrasystoles  which  are  followed  by  compensatory  pauses  are 


PLATE   IX 


-*+ 

--< 

-    r 

_!_ 

Fig.  76.  —  Electrocardiogram  showing  diphasic  TI,  negative  Til  and  Till.      From  a 
patient  with  hypertension  and  myocarditis. 


Fig.  95.  —  Auricular  extrasystoles. 


Fig.  96.  —  Auricular  extrasystoles.      The  conduction  time  (P'R')  is  slightly  prolonged. 


Fig.  97. — Auricular  extrasystoles  superimposed  upon  the  T  wave  (TP').     The  prema- 
ture auricular  contraction  P-  is  followed  by  an  ectopic  ventricular  beat  (V.Ex). 


Fig.  98.  —  Auricular  extrasystole  showing  the  superposition  of  P  and  T  waves  (P'T). 


THE   ARRHYTHMIAS 


53 


54 


CLINICAL   CARDIOLOGY 


easily  diagnosed ;  when  interpolated,  their  recognition  is  more  difficult. 
If  the  premature  contraction  is  frustrane,  that  is,  if  its  course  in  the 
ventricle  is  improperly  directed  or  not  sufficiently  powerful  to  open  the 
aortic  valves,  there  is  no  corresponding  pulse  beat  at  the  wrist ;  other- 
wise, the  extrasystole  causes  a  stronger  or  weaker  pulse.  At  the  heart 
one  or  two  sounds  of  varying  intensity  accompany  the  premature  con- 
traction. If  the  extrasystole  opens,  and  the  aortic  valves  subsequently 
close,  a  premature  first  and  a  premature  second  sound  is  heard ;  if  the 
ventricular  pressure  remains  lower  than  the  aortic,  a  premature  first 
sound  alone  is  heard.  Only  rarely  is  this  sound  too  faint  to  be  audible. 
While  graphic  methods  of  registration  are  required  to  determine  the 
exact  length  of  the  compensatory  pause,  distinct  shortening  of  the  latter 
is  readily  determined  by  palpation  at  the  wrist.  Marked  differences 
in  the  duration  of  the  compensatory  pauses  characterize  auricular, 
rather  than  ventricular,  extr asystoles.  The  likelihood  of  a  premature 
contraction  being  auricular  is  increased  if  it  produces  a  fairly  strong  pulse 
beat ;  the  weaker  wave  is  more  characteristic  of  a  ventricular  premature 
contraction.  It  is  occasionally  possible  to  distinguish  auricular  from 
ventricular  extrasystoles  by  observation  of  the  jugular  pulsations,  for 
in  the  ventricular  type  a  large  summation  wave  (corresponding  to  the 
polygraphic  a  and  c'  waves)  may  occasionally  be  seen. 

Coupled  Rhythm.  —  Its  diagnosis  rests  upon  the  clinical  recogni- 
tion of  regularly  recurring  extrasystoles.  The  distinction  from  coupled 
rhythm  accompanying  auricular  fibrillation  depends  upon  the  clinical 
characteristics  of  the  latter  (q.v.). 

Irregularly  occurring  extrasystoles  of  varying  force  in  a  heart 
beating  rapidly  are  most  apt  to  be  confused  with  auricular  fibrillation. 
The  only  differential  guide  is  observation  of  the  jugular  and  of  carotid 
beats;  even  here,  differentiation  is  often  impossible  because  of  the 
rapidity  of  the  pulsatile  waves  which  makes  it  extremely  difficult  for  the 
eye  to  decipher  them. 

A  II.     Paroxysmal  Tachycardia  of  Auricular  Origin 

The  term  Simple  Tachycardia  should  be  applied  to  the  common 
acceleration  of  the  normal  sinus  rhythm ;  the  usual  ventricular  rate  is 


j^^jiJpt^M  m 


Fig.  100. 

Figs.  100,  101.  —  Varying  ventricular  rates  from  a  case  of  exophthalmic  goiter  recorded 
on  different  days.  When  the  rate  is  150  per  minute  (Fig.  100),  the  a-c  interval  is  nor- 
mal. When  the  rate  is  225  (Fig.  101),  the  a-c  interval  is  slightly  diminished ;  the  dia- 
stole is  entirely  abolished.     The  a  wave  falls  with  the  v  of  the  preceding  beat. 


THE   ARRHYTHMIAS 


55 


Fig.  102.  — Paroxysmal  tachycardia.  On- 
set and  offset  not  recorded.  Shortened 
conduction  time.  The  a  wave  falls  with 
the  preceding  v. 


between  110  and  130  per  minute.    Paroxysmal  tachycardia  of  auricular 
origin  consists  essentially  in  auricular  extrasystoles  coming  in  attacks. 

It  is  accompanied  bv  an  extreme, 

abrupt  acceleration  of  the  normal 
rhythm,  with  an  abrupt  termina- 
tion and  return  to  the  normal.  It 
may  last  minutes,  hours,  or,  more 
rarely,  days.  Like  the  single  au- 
ricular extrasystole,  it  is  basically 
due  to  abnormal  passage  of  the 
impulse.  Graphically  studied,  the 
attack  is  seen  to  begin  with  a  definite  "  onset  "  and  to  end  with 
a  definite  "offset."  Typical  attacks  are  initiated  and  terminated  by  ex- 
trasystoles. The  ventricu- 
lar rate  usually  varies  from 
170  to  200  per  minute.  The 
rapid  heart  action  of  simple 
and  paroxysmal  tachycardia 
is  usually  at  the  expense 
of  diastole  (Figs!  100-102). 
The  conduction  time  as  well 
is  occasionally  diminished 
(Figs.  102-106).  In  a  large 
proportion  of  cases  of  ex- 
ophthalmic goiter,  I  found  diminished  auriculo-ventricular  conduction 
time  despite  the  fact  that  ventricular  acceleration  was  not  extreme 
(Figs.  103,  106).  •       ....  jh  .  ,   T       .    .    .    .   M   „   .  ^- 

Studied    electrocardiographi-     ^|ri\^^'^^'^^^  ^"~" 
cally,  it  is  found  that  the  par-  /        I       ''  j 

oxysms    usually    originate    from  Raumau   $ate  ^  ia.o  pf 

an  ectopic  auricular  focus.    When  ;        *         ;         i 

the  change  in  the  auricular  com- 
plex is   not   marked,   an   origin 
close  to  the  normal 
sinus    area     is     as-      '  *ft   "— 
sumed.      When    de 
viated  negatively,  it 
indicates    an    origin 
in   the    lower    part 
of      the      auricular 
musculature. 

Clinical  Recog- 
nition of  Simple 
Tachycardia  and  of  Paroxysmal  Tachycardia  of  Auricular  Origin.  — 
The  former  refers  to  rhythmic  pulse  and  ventricular  action  at  the  rate 
of  about  120  or  more  per  minute.     Its  recognition  is  usually  simple. 


RADIAL         RATE.       .130 


Fig.  103.  —  Exophthalmic  goiter.  Ventricular 
rate,  130  per  minute.  Very  much  shortened 
conduction  time  (a—  v  interval)  despite  only 
moderate  acceleration  (simple  tachycardia). 


Fig.  104. 


fioJlaLA^fcfZo/AV 


Fig.  105. 

Figs.  104,  105.  —  Exophthalmic  goiter.  Ventricular  rate, 
120  per  minute ;  simple  tachycardia ;  shortened  a-c 
interval. 


56 


CLINICAL   CARDIOLOGY 


It  may  be  confused  with  the  rapid  heart  action  of  auricular  fibrillation, 
but  the  pulse  of  the  latter  will  be  found  arrhythmic  upon  longer  or 
shorter  observation.     Paroxysmal  (auricular)  tachycardia  is  recognized 

by  its  characteristic  onset  and  offset, 

an  extrasystole  with  its  compen- 
satory pause  initiating  and  complet- 
ing the  typical  attack.  These  data, 
however,  can  rarely  be  obtained  by 
direct  clinical  observation.  In  most 
instances  we  shall  have  to  depend 
upon  the  history  of  a  sudden  be- 
ginning and  termination  of  the  at- 
tack ;  in  addition,  we  may  obtain  a 
fairly  accurate  description  of  the  oc- 
currence of  an  extrasystole  by  such  accounts  as  :  "  The  heart  stops  for 
a  moment,"  or :  "  There  is  a  momentary  faint  feeling  in  the  chest 
before  or  after  the  palpitation."  Immediately  or  very  soon  after  the 
attack,  moderate  tachycardia  or  even  extrasystoles  can  often  be  evoked 
by  such  maneuvers  as  rapid  breathing,  exercises,  sudden  change  of 
position,  etc. 

The  differentiation  of  paroxysmal  tachycardia  from  auricular  flutter 
(q.v.)  and  from  the  tachycardial  attacks  accompanying  auricular  fibrilla- 
tion (q.v.)  will  be  discussed  under  those  arrhythmias. 


RADtAu      RATfc     -     130     PER     M- 


Fig.  106.  —  Exophthalmic  goiter.  Ven- 
tricular rate,  130  per  minute ;  simple 
tachycardia ;  a-c  considerably  de- 
creased. 


A  III.     Auricular  Incoordination 

It  will  be  noted  that  the  three  types  of  arrhythmia  to  be  described  — 
fibrillation,  flutter,  and  the  intermediate  form  —  result  primarily  from 
auricular  incoordination.  An  extreme  degree  of  inchoate  auricular 
activity  results  in  auricular  fibrillation.  "When  incoordinate  activity 
is  less  marked,  it  results  in  auricular  flutter  (or  auricular  t  achy  systole). 
There  exists,  also,  an  intermediate  form. 


A  III.     (1)  Auricular  Fibrillation 

This  constitutes  approximately  three  quarters  of  all  kinds  of  arrhyth- 
mias. We  now  know  that  the  great  majority  of  cases  which  Mackenzie 
called  nodal  rhythm  belong  to  this  category.  When  auricular  fibrillation 
is  typical,  ventricular  activity  is  completely  irregular  in  rhythm  and 
force,  so  that  no  two  successive  beats  are  alike.  If  induced  experimen- 
tally in  animals,  the  auricles  show  irregular  tremulous  fibrillating  activ- 
ity ;  sometimes  and  in  some  parts  of  the  auricle  the  fibrillation  is  fine, 
and  at  other  times  and  other  places  it  is  coarse.  There  is  no  unity  in 
auricular  contractility,  although  occasionally  waves  of  fibrillation  pro- 
ceed with  a  fair  degree  of  regularity  over  the  entire  musculature.  The 
auriculo-ventricular  conduction  system  is  bombarded,  as  it  were,  by 
numerous  irregular  impulses,  only  some  of  which  can  pass  through  the 


THE   ARRHYTHMIAS 


57 


Figs.  107-120.  —  Different  types  of  polygrams  of  auricular  fibrillation.  The  radial 
tracings  show  varying  degrees  of  irregularity  of  rhythm  and  force  of  the  pulse  beats ; 
some  are  grossly  irregular  (for  example,  Figs.  108,  114,  117)  ;  others  more  nearly  ap- 
proach the  normal  pulse  rhythm  (Figs.  113,  118,  120).  The  jugular  tracings  are  of 
the  most  varied  types.  Their  pathognomic  characteristic  is  the  absence  of  the 
rhythmic  a  wave  regularly  preceding  the  c.  Small  waves  preceding  the  c  are  some- 
times observed  (Figs.  107,  108,  110),  but  their  incidence  and  size  are  irregular.  The 
c  wave  may  be  split  (Figs.  115,  119)  or  may  form  a  combined  wave  with  the  v  (Figs. 
118-120),  especially  when  ventricular  action  is  slow. 


Fig.  108 


Fig.  111. 


Fig.  112. 


58 


CLINICAL  CARDIOLOGY 


junctional  tissue  and  excite  the  ventricle  to  irregular  and  discordant 
response. 

The  polygram  corresponds  to  the  pathological  physiology  just 
described.  In  typical  instances  the  radial  tracing  shows  gross  and 
complete  irregularity  in  the  force  and  rhythm  of  the  radial  beats ;    in 


Fig.  113. 


Fig.  114. 


Fig.  115. 


Fig.  116. 


the  jugular,  the  representative  of  orderly  rhythmic  auricular  contrac- 
tion, the  a  wave,  is  absent  (Figs.  107-121).  It  is  said  that  fibrillation  is 
sometimes  sufficiently  coarse  to  produce  small  fibrillary  reflux  waves 
in  the  superior  vena  cava  and  jugular  bulb ;  these  are  then  indicated  in 
the  tracings  as  irregular  wave-like  lines.  When  found  in  mitral  stenosis 
with  a  marked  diastolic  thrill,  it  seems  to  me  that  such  fibrillary  waves 
may  be  due,  not  to  auricular  fibrillation,  but  to  turbulent  diastolic  ven- 
tricular eddies  propagated  as  small  waves  from  vibrations  of  the  stiffened 
mitral  valves,  through  the  heart  to  the  superior  vena  cava  and  jugular 


THE  ARRHYTHMIAS 


59 


0 


01 


■I 


60 


CLINICAL  CARDIOLOGY 


veins.  Figure  122  shows  fibrillary  waves  from  a  case  of  mitral  stenosis 
with  a  loud,  exceedingly  rough,  diastolic  murmur  and  thrill.  There 
was,  in  addition,  a  short,  sharp,  regularly  recurring  presystolic  wave  (Fig. 


Fig.  121.  — Auricular  fibrillation,  anacrotic  radial  pulse. 


Fig.  122.  —  Auricular  fibrillation  with  mitral  stenosis  showing  presystolic  (x)  and  fibrillary 

(/)  waves. 


Fig.  123. 


Fig.  124. 

Figs.  123,  124.  —  Auricular  fibrillation  ;    sharp  fall  of  pressure  following  the  ventricular 
filling  wave.    In  Fig.  124,  the  radial  pulse  is  quite  rhythmical.    Digitalis  had  been  given. 


122,  x)  whose  etiology  is  not  clear.     Electrocardiograms  taken  at  that 
time  preclude  the  possibility  of  its  being  an  auricular  wave. 

In  some  of  the  jugular  tracings  of  auricular  fibrillation,  a  sharp  rise 
and  subsequent  fall  of  pressure  succeeding  the  v  wave  is  found  (Figs.  123- 
124).  As  already  indicated,  a  completely  irregular  pulse  accompanies 
auricular  fibrillation  in  the  great  majority  of  cases  (Figs.  125-129). 


THE   ARRHYTHMIAS 


61 


9> 


£ 


c=.    .3 


62 


CLINICAL  CARDIOLOGY 


Very  rarely  the  pulse  becomes  absolutely  regular  as  the  result  of  digitalis 
medication,  though  fibrillation  continues  (Fig.  124). 

Corresponding  to  the  state  of  incoordinate  auricular  activity  char- 
acteristic of  auricular  fibrillation,  there  is  in  the  electrocardiogram  an 
absence  of  regularly  recurring  auricular  deviations   (P   waves).     In 


Fig.  133.  —  Fine  fibrillation  waves. 


Jl^T^^gi^gU^ 


their  place,  there  are  undulations,  representing  fibrillation,  at  rates 
between  350  and  900  per  minute.  These  fibrillation  waves  vary  con- 
siderably in  type.  In  short  runs  they  may  resemble  the  regular  and 
rapid  auricular  activity  of  flutter ;  at  other  times  the  waves  are  coarse 
and  arrhythmic,  or  are  so  small  as  to  be  scarcely  distinguishable  as  sepa- 
rate deviations.  Examples  of  these  various  tvpes  are  shown  in  Figs.  130, 
131  (Plate  X),  132,  134,  135,  137  (Plate  XI),  133,  136,  138,  139.    At 

present  there  is  no 
clinical  distinction 
based  upon  these  dif- 
ferences. 

In  older  people 
with  cardiosclerosis, 
or  as  a  residt  of  digi- 
talis medication  in 
others,  the  pulse  and 
heart  action  may  be 
fairly  regular  in  force 
and  rhythm,  so  that 
graphic  tracings  are 
required  in  order  to  establish  the  diagnosis  of  fibrillation.  In  another 
clinical  type  of  fibrillation,  the  pulse  rate  varies  between  ISO  and  225 
per  minute,  and  is  small  in  volume  and  easily  compressible.  L^pon 
palpation,  the  individual  beats  appear  equal  in  force.  Clinically,  this 
resembles  paroxysmal  tachycardia.  Electrocardiographically,  it  is  dis- 
tinguished from  the  latter  bv  the  absence  of  P  waves  and  by  the 
absence  of  an  "  onset  "  and  "'offset"  (Fig.  137,  Plate  XI). 

Ectopic  beats  are  sometimes  present  in  auricular  fibrillation  (Fig. 
138,  Ec).  They  are  erroneously  called  extrasystoles  ;  the  latter  term  is 
properly  applicable  only  to  premature  beats  which  disturb  an  otherwise 


Fig.  136.- 


Fairly  regular  fibrillation  waves  in  parts  of  LI  I 
and  LIII. 


PLATE  X 


PLATE   XI 


-  j -|  ,        j  : 


Fig.  132.  —  Fairly  regular  fibrillation  waves  which  at  times  resemble  flutter. 


: *^*        '    *+ 

»       <** 

.♦.t     •               

— — - 

t 

— 

*^ 

~r~ 

_ 

Fig.  134.  —  Various  types  of  fibrillation  waves,  coarse  and  fine,  in  the  same  lead. 


Fig.  135.  —  Very  fine  fibrillation  waves 


w^,ww 


z^  : 

r j 

:  z: :t ..: 

•  > 

j:    j 

— 1- 

1— 1— 

r 

Mi 

■*Uufi 

Fig.  137.  —  Auricular  fibrillation  showing  tachycardia  in  L  I.      Note  the  varying  rates 

of  ventricular  rapidity. 


THE  ARRHYTHMIAS 


63 


regular  rhythm,  and  not  to  beats  occurring  in  the  complete  irregularity 
of  auricular  fibrillation. 

Transient  Auricular  Fibrillation.  —  Only  exceptionally  is  it  possible 
to  note  sudden  transitions  from  normal  rhythm  to  auricular  fibrillation. 


i)  ij 

;j:p|:g|-  if-il 

f-H  |--jjttHf 

,  ::~.t 

w 

.ym 

ffi 

w 

raWpiipip 

sa|Fc± 

m* 

Ji-i 

f 

Ifflf 

:::u„ 



-   - 

S 

TtfrS  s  |ff  Ifft  "TT 

T 

Fig.  13S.  —  Auricular  fibrillation  with  ectopic  beat  (Ec). 


Such  attacks  may  be  the  result  of  digitalis  therapy.  They  are  also 
found  in  exophthalmic  goiter  or  at  the  crises  of  severe  infections  (for  ex- 
ample, in  pneumonia).  They  are  by  no  means  infrequent  in  older  pa- 
tients with  cardiosclerosis,  in  whom  hypertension  is  a  marked  clinical 
feature.  Attacks  of  auricular  fibrillation,  in  addition,  occur  in  the 
decompensatory  stages  of  valvular  disease.  Its  occurrence  with  au- 
ricular flutter  has  already  been  pointed  out.  Its  presence  in  a  patient 
with  no  temperature  and  with  no  sign  of  organic  cardiovascular  disease 
is  very  rare.  Figure  140 
(Plate  XII)  is  an  example.  It 
was  taken  from  a  child  of  eight, 
not  neurotic,  who  had  had  sev- 
eral attacks  of  tonsillitis.  Ton- 
sillectomy was  performed  two 
years  before.  Shortly  before 
she  came  under  my  observa- 
tion, she  suddenly  felt  her 
heart  "jump":  this  "jump- 
ing "  sensation  has  since  been 
occasionally  repeated.  There 
were  no  gastric  symptoms. 
The  child  was  somewhat 
anemic  and  undersized.  There 
were  no  signs  of  decompensation.  The  urine  contained  no  abnormal 
elements.  There  was  a  very  soft  faint  systolic  murmur,  of  functional 
nature,  at  the  apex ;  the  murmur  was  not  transmitted.  The  electro- 
cardiogram (Fig.  140,  LI II)  shows  the  above-mentioned  short  run  of 
auricular  fibrillation  (A.F  .  .  .  A.F)  following  the  ventricular  extra- 
systole  (V.Ex).  In  addition,  there  is  fairly  marked  sinus  arrhythmia. 
There  are  several  ventricular  extrasystoles  (V.Ex),  in  some  of  which 
the  auricular  beat  is  seen  as  a  separate  deviation  (P').  There  is  also 
an  auricular  extrasy stole  of  sinus  origin  with  an  abnormal  ventricular 
complex  (LI,  A. Ex) ;    it  is  not  followed  by  a  compensatory  pause. 


Fig.  1 39.  —  Auricular  fibrillation  with  coarse 
fibrillation.     (Courtesy  of  Dr.  A.  E.  Cohn.) 


64  CLINICAL   CARDIOLOGY 

Clinical  Recognition  of  Auricular  Fibrillation.  —  The  pulse  and  ven- 
tricular irregularity  of  typical  auricular  fibrillation  is  sufficiently  obvious 
to  be  readily  manifest.  At  the  apex  there  is  marked  irregularity  in  force 
and  rhythm  of  the  heart's  action.  Sometimes  scarcely  two  beats  are 
alike ;  sometimes  there  is  fairly  regular  heart  action  lasting  several 
seconds  or  longer.  At  the  wrist,  if  all  beats  come  through,  the  pulse, 
completely  irregular,  takes  on  a  helter-skelter  characteristic.  In  the 
neck  the  carotids  are  correspondingly  irregular ;  the  jugular  pulsations 
are  usually  too  rapid  to  be  individually  identified.  If  there  are  many 
frustrane  ventricular  contractions  (so-called  pulse  deficit),  the  radial 
seems  fairly  regular  in  force  and  rhythm,  for  it  is  mainly  the  small  and 
weaker  beats  which  produce  the  picture  of  complete  irregularity ;  aus- 
cultation at  the  cardiac  apex  will  readily  reveal  these  small,  numerous, 
and  discordant  beats.  Indeed,  in  thin  persons,  inspection  of  the  apical 
region  shows  the  characteristically  arrhythmic  ventricular  action  of 
auricular  fibrillation. 

The  ectopic  beats  in  auricular  fibrillation  (sometimes  erroneously 
called  "  extrasystoles ")  can  occasionally  be  recognized  even  when 
ventricular  action  is  rapid  and  irregular,  because  they  are  commonly 
followed  by  momentary  (not  compensatory)  pauses,  and  by  beats  much 
louder  and  stronger  than  the  preceding.  In  the  tachycardial  attacks 
occurring  with  auricular  fibrillation,  there  is  no  onset  or  offset,  the  beats 
are  sufficiently  irregular  in  force  and  rhythm  to  be  palpable  and  are  apt 
to  be  interspersed  with  the  typical  gross  irregularity  of  auricular  fibrilla- 
tion; after  the  attacks  a  completely  irregular  pulse  is  again  present. 
These  are  data  which  serve  in  the  differentiation  between  this  type  and 
the  paroxysmal  tachycardia  already  discussed. 

In  auricular  fibrillation  with  coupled  rhythm  and  fairly  slow  and 
regular  ventricular  activity  and  pulse,  or  in  those  rare  instances  of  a 
perfectly  regular  pulse  following  digitalis  medication,  differentiation 
from  the  normal  or  from  extrasystolic  arrhythmia  can  only  be  made  by 
direct  observation  of  the  jugular  pulsations.  If  distinct  auricular  waves 
can  be  recognized,  their  presence  serves  to  exclude  fibrillation. 

A  III  (2).    Auricular  Flutter.  —  Auricular  Tachysystole 

In  this  type  the  auricles  beat  regularly  and  rapidly  from  225  to  350 
times  per  minute.  Since  the  ventricle  cannot  respond  at  a  like  rate, 
heart  block  (q.v.),  incomplete  or  complete,  results.  If  the  block  be 
incomplete  at  a  2 :  1,  3 : 1,  or  4: 1  ratio,  the  pulse  remains  regular,  the 
rate  depending  upon  the  ratio.  If  incomplete  heart  block  be  present 
with  a  constantly  varying  auriculo-ventricular  ratio,  the  pulse  becomes 
irregular.  The  polygraphic  recognition  of  auricular  flutter  may  be  diffi- 
cult, for  the  auricular  waves  are  often  small  and  distorted  by  respiration. 
Lewis  has  pointed  out  that  under  these  circumstances  the  arrhythmic 
groups  of  radial  beats  form  exact  multiples,  so  that  auricular  flutter 


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THE   ARRHYTHMIAS 


65 


may  be  diagnosed  from  the  radial  curve  alone.  I  have  not  found  this 
to  apply  to  some  cases  of  flutter  that  I  measured  and  attempted  to  diag- 
nose in  this  manner.  When  auricular  waves  are  well  marked  (Figs.  141 
A  and  B,  Fig.  142),  flutter  is  readily  recognized.  In  the  interpretation 
of  the  degree  or  type  of  block,  it  must  be  remembered  that,  when  incom- 
plete, the  a-c  interval  may  be  abnormally  prolonged ;  this  may  give 
the  appearance  of  shortened  conduction  time,  for  the  ventricle  has 


Fig.  141.  —  Tracing  of  auricular  flutter.  A  and  B  were  obtained  on  different  days. 
a,  b,  c  are  continuous.  In  A,  the  auricular  rate  is  210 ;  in  B,  245  per  minute.  The  num- 
bers on  the  radial  beats  denote  their  respective  lengths  in  f  seconds.  The  block  is 
complete  in  A  (a  and  b)  and  changes  from  incomplete  to  complete  in  c.  The  block  is 
incomplete  in  B  (a  and  part  of  b)  and  then  later  becomes  complete. 

probably  responded,  not  to  the  immediately  preceding  auricular  beat, 
but  to  the  one  previous  (indicated  by  arrows,  Figs.  142,  143).  The 
conduction  time  is  approximately  .4  second.  Partial  heart  block  with 
a  3  :  1  rhythm  is  shown  in  Fig.  143.  The  pulse  is  almost  regular 
throughout,  though  there  are  shorter  and  longer  beats  indicative  of 
change  in  the  auriculo-ventricular  ratio.  In  other  instances  of  flutter 
there  may  be  found  a  change  from  partial  to  complete  block,  or  the 
reverse  (Fig.  141). 


66 


CLINICAL  CARDIOLOGY 


An  electrocardiographic  example  of  incomplete  and  complete  block 
in  the  same  electrocardiogram  (Fig.  144,  Plate  XIII)  is  shown.  Rapid, 
regular  auricular  activity  is  best  seen  in  LII  and  III.  The  ventricular 
rate  was  75,  the  auricular  300  per  minute.  Incomplete  block  at  a  4  :  1 
ratio  was  present.  The  P  and  T  waves  are  occasionally  superimposed. 
The  P  waves  are  contiguous  and  distinct  in  LII  and  III.  They  are 
scarcely  discernible  in  LI.     This  is  a  characteristic  of  auricular  flutter. 


Fig.  142.  —  Auricular  flutter.  The  numbers  on  the  radial  beats  denote  their  respective 
lengths  in  J  seconds.  The  auricular  impulse  and  its  corresponding  ventricular  response 
are  shown  by  arrows. 


At  a  later  date,  the  auricular  speed  was  the  same,  300  per  minute.  The 
ventricular  rate  varied  from  60  to  100  per  minute.  There  is  no  group 
proportion  discoverable  in  the  varying  ventricular  rates  ;  complete  heart 
block  is  present.  After  10  drachms  of  the  tincture  of  digitalis,  given 
over  a  period  of  10  days,  there  was  no  diminution  of  auricular  speed ; 
the  ventricular  activity  was  arrhythmic.  There  was  also  a  difference  in 
the  heights  of  the  R  deviations.  This  difference  was  not  of  respiratory 
origin  ;  it  may  have  been  due  to  differing  degrees  of  ventricular  excitabil- 
ity from  digitalis  medication.  The  electrocardiogram  (Fig.  144,  Plate 
XIII)  was  derived  from  a  case  of  acute  endo-pericarditis  without  de- 
compensation ;  flutter  developed  during  the  course  of  acute  rheumatic 
joint  manifestations.  In  this  instance,  digitalis  did  not  have  the  effect 
usually  found  in  flutter  with  cardiac  decompensation,  viz. :  first,  auricu- 
lar fibrillation ;  later,  the  resumption  of  normal  rhythm  with  cessation 
of  medication.  As  stated,  there  was  no  decompensation  in  this  case. 
The  rhythm  became  normal  only  when  the  joint  symptoms  subsided,  the 
temperature  reached  the  normal  and  the  endocardial  lesion  became 
quiescent.     From  the  clinical  course,  I  conclude  that  the  exciting  cause 


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THE   ARRHYTHMIAS 


67 


of  the  flutter  was  the  acute  endocarditis.  In  what  man- 
ner the  latter  produced  the  arrhythmia  it  is  impossible 
to  state.  One  year  after  the  onset  of  the  disease,  the 
rhythm  was  still  normal,  the  signs  of  the  endocardial 
lesion  (mitral  regurgitation)  were  the  same. 

Clinical  Recognition  of  Auricular  Flutter.  —  In  the 
exceptional  instances  of  this  arrhythmia  in  which  the 
veins  of  the  neck  are  tremendously  distended  by  each 
auricular  systole,  the  diagnosis  becomes  at  once  evident 
on  inspection  and  estimation  of  the  rapidity  of  the  jugular 
pulsations.  The  latter,  however,  are  more  often  minute 
and  scarcely  distinguishable  as  separate  beats.  Though 
not  thus  definable  as  individual  waves,  the  jugular  pulsa- 
tions are  often  sufficiently  distinct  for  one  to  note  that 
their  number  greatly  exceeds  that  of  the  ventricular  con- 
tractions. In  this  manner  the  diagnosis  of  flutter  may 
occasionally  be  ventured ;  but  most  diagnostic  reliance 
must  finally  be  placed  upon  recognition  of  heart  block 
with  the  varying  auriculo-ventricular  ratios  typical  of 
flutter.  If,  for  example,  incomplete  heart  block  at  a 
constant  ratio  is  present,  the  pulse  and  heart  action  are 
regular,  the  rate  usually  being  between  90  and  120.  If 
the  auriculo-ventricular  ratios  be  inconstant  and  con- 
stitute changing  multiples,  as  from  2:1  to  4:1  or  the 
reverse,  the  diagnosis  of  flutter  can  be  made  from  the 
fact  that  the  ventricular  pauses  also  constitute  multiples. 
If  the  auriculo-ventricular  ratio  constantly  varies,  or  if 
complete  heart  block  is  present,  ventricular  action  and 
pulse  become  arrhythmic,  and  clinically  resemble  the 
irregular  action  of  frequent  extrasystoles  or  of  auricu- 
lar fibrillation.  The  differentiation  can  then  only  oc- 
casionally be  made  from  the  latter,  by  the  absence  of  its 
characteristic  jugular  pulse ;  from  the  former,  by  the 
absence  of  compensatory  pauses. 

A   III.     (3)  Incoordination  Intermediate  between 
Flutter  and  Fibrillation 

In  a  few  instances,  I  have  observed  a  state  of  irregu- 
lar auricular  activity  which  may  be  regarded,  I  believe, 
as  an  intermediate  stage  of  incoordination  between  flut- 
ter and  fibrillation.  The  auricular  rate  was  usually 
between  110  and  150;  the  beats,  as  shown  by  the  differences  in 
the  auricular  complexes,  came  from  many  scattered  ectopic  foci ;  the 
auricular  rhythm  was  irregular.  The  ventricular  rhythm  was  also 
irregular,  the  rate  usually  between  100  and  120.     Many  of  the  ventric- 


€ 


o  o 


68 


CLINICAL   CARDIOLOGY 


ular  electrocardiographic  complexes  varied  in  the  length  o£  their  devia- 
tions ;  very  few  ventricular  extrasystoles  were  present ;  the  picture 
betokened  impulses  following  many  vicarious  paths  in  the  ventricle. 
Although  the  electrocardiographic  picture  of  the  ventricular  arrhythmia 
was  not  as  distinct  as  was  the  case  with  the  irregular  (ectopic)  auricular 
activity,  it  seemed  probable  that  ventricular  arrhythmia  was  likewise 
due  to  incoordinate  activity,  but  of  a  degree  considerably  less  than  in 
ventricular  fibrillation  (q.v.). 

The  patients  who  presented  this  rare  and  interesting  arrhythmia  were 
in  the  agonal  stages  of  pneumonia  or  of  cardionephritis.  It  seemed 
possible,  from  the  clinical    pictures  presented,   that    several   factors 

deserved  etiological  con- 
sideration :  e.g.  in  pneu- 
monia, the  toxins;  in 
cardionephritis,  retained 
abnormal  products.  In 
all,  there  were  probably 
changes  in  the  intra- 
cardiac circulation  which 
profoundly  affected  the 
nutrition  of  the  general 
musculature,  as  well  as 
of  the  auriculo-ventricu- 
lar  conduction  system. 

Although,  as  indi- 
cated, irregular  auricu- 
lar activity  may  be  due 
to  two  fundamentally 
different  causes  (abnor- 
mal passage  of  impulses 
and  auricular  incoordi- 
nation), it  is  interesting 
to  note  the  gradations 
and  transitions  in  auricular  irregularity.  First  are  the  isolated  auricular 
extrasystoles.  These,  if  numerous  and  originating  outside  the  sinus 
area,  give  rise  to  auricular  tachycardia.  The  rate  is  then  between  150 
and  225.  If  auricular  speed  be  increased  from  225  to  350  per  minute, 
flutter  results.  This  appears  to  be  the  limit  of  regular  auricular  activ- 
ity in  man.  Any  further  increase  in  rate  results  in  irregular  activity  — 
auricular  fibrillation.  The  fibrillation  waves  may  be  as  frequent  as 
900  per  minute.  In  some  instances  it  is  possible  to  observe  a  transition 
from  auricular  flutter  to  fibrillation  (Fig.  145).  Between  flutter  and 
fibrillation  is  the  intermediate  type  of  inchoate  auricular  activity  just 
described. 


Fig.  145.  —  Paroxysmal  auricular  tachycardia.  F .  . .  F 
{L  III)  shows  change  of  paroxysmal  tachycardia  to 
auricular  fibrillation  (absence  of  regularly  recurring 
auricular  complexes).     (Courtesy  of  Dr.  A.  E.  Cohn.) 


THE   ARRHYTHMIAS 


69 


A'.     NODAL   EXTRASYSTOLES 

Premature  contractions  having  their  origin  in  the  auriculo- 
ventricular  node  are  called  nodal  extrasystoles.  The  auricular  and 
ventricular  im- 
pulses start  si- 
multaneously, or 
almust  simul- 
taneously, from 
their  nodal 
origin.  Hence, 
in  the  jugular 
tracings,  the  a 
and  c  waves, 
and,  in  the  elec- 
trocardiogram, 
the  P  and  R 
waves  fall  coinci- 
dentally,  or 
nearly  coinci- 
dentallv  (Fig. 
146).  "  In  the 
phlebogram,  a 
large  summation 
a  +  c    wave    is 

produced  (Figs.  147,  148) ;  in  the  electrocardiogram,  the  small  P  is  often 
lost  in  the  larger  R  complex. 


Fig.  146.  —  Nodal  extrasystole  showing  coincidence  of  P  and  R 
waves.     (Courtesy  of  Dr.  A.  E.  Conn.) 


Fig.  147.  —  Xodal  extrasystole.  This  is  graph- 
ically illustrated  by  the  almost  synchronous 
occurrence  of  the  foot  points  of  A'c'. 


Fig.  148.  —  Nodal  extrasystole  which 
has  produced  no  pulse  wave.  (Frus- 
trane  contraction.) 


B.    VENTRICULAR  ARRHYTHMIAS 


I.     Ventricular  Extrasystoles 

As  with  the  auricular  type,  ventricular  extrasystoles  depend  upon  the 
abnormal  passage  of  the  impulse. 

The  main  distinction  between  heterogenetic  (aberrant)  ventricular 
beats  and  those  arising  in  the  auriculo-ventricular  node  —  true  idio- 
ventricular rhythm  —  is  one  of  rate.  This  node  originates  rhythmical 
contractions  at  a  frequency  between  25  and  40  per  minute  (heart block). 


70 


CLINICAL   CARDIOLOGY 


The  rate  of  extrasystolic  ventricular  rhythm  is  between  130  and  200 
per  minute. 

In  ventricular  extrasystoles  (Fig.  82)  the  auricle  follows  its  normal 
rhythm  and  contracts  when  the  ventricle  is  in  a  refractory  state,  and, 


K  +    K    <  /iS  +>  c  f> 


Figs.  149,  150.  —  The  ventricular  extrasystole  plus  the  compensatory  pause  is  slightly 
greater  than  two  rhythmic  beats.      (Increased  compensatory  pause.) 

as  a  result,  there  is  no  ventricular  response  until  the  next  succeeding 
ventricular  contraction.  Thus  the  time  of  ventricular  prematurity, 
added  to  the  '  compensatory '  pause,  equals  two  rhythmic  beats.     This 


Fig.  151.  —  Ventricular  extrasystole  plus  compensatory  pause  is  less  than  two  rhythmic 
beats  (diminished  compensatory  pause). 

fact  is  of  value  in  the  recognition  of  ventricular  extrasystoles  from  radial 
tracings  alone,  or  in  polygraph ic  tracings  in  which  the  jugular  is  not 
sufficiently  clear  to  be  of  value.     In  auricular  extrasystoles,  both  cham- 


tt  v  £# 


3lc  V  (L 


Fig.  152.  —  Ventricular  extrasystole  without  compensatory  pause. 

bers  contract  prematurely  and  the  succeeding  pause  may  or  may  not 
be  '  compensatory  '  (Fig.  81).  Ventricular  extrasystoles,  likewise,  are 
sometimes  followed  by  pauses  which  are  not  exactly  compensatory  in 


THE   ARRHYTHMIAS  71 

length  (Figs.  149-152).  Occasionally  premature  contractions  occur  so 
late  that  they  lose  their  characteristic  "  prematurity  "  (Fig.  153).  The 
amplitude  of  the  radial  beat  following  the  extrasystolic  pause  in  any 


JUdUL 


Fig.  153.  —  Extrasystole  which  is  not  '  premature.'    r'  is  greater  than  P  (the  pause  follow- 
ing extrasystole). 

type  of  premature  contraction  is  usually  larger  than  that  of  the  normal 
beat,  and  expresses  graphically  its  greater  strength  (Figs.  83,  85,  153) ; 
this  is  sometimes  regarded  as  indicative  of  favorable  cardiac  recupera- 
tive power. 

B  II.     Interpolated  Ventricular  Extrasystoles 

When  the  cardiac  rate  is  slow,  ventricular  extrasystoles  do  not  always 
interfere  with  the  time  of  the  next  normal  ventricular  contraction; 
these  are  called  "  interpolated."  This  type  of  premature  contraction 
occurs  in  the  course  of  normal  rhythm,  and  is  not  followed  by  a  com- 
pensatory pause.  Such  extrasystoles  are  found  in  mid-diastole  and  in 
groups,  rarely  as  isolated  phenomena.  Figure  56  (Plate  VII)  is  there- 
fore of  interest  because  it  shows  a  single  interpolated  extrasystole 
(L  II  Ex).  The  electrocardiogram  was  derived  from  a  male  patient 
54  years  old,  who  presented  extreme  decompensation.  He  had  had 
syphilis  30  years  before.  The  Wassermann  blood  reaction  was  positive. 
He  had  severe  myocarditis  and  marked  left  ventricular  hypertrophy. 
Fluoroscopy  and  radiography  demonstrated  aneurismal  dilatation  of 
the  entire  thoracic  aorta.  Under  vigorous  antiluetic,  and  the  usual 
treatment  for  decompensation,  the  patient  improved  to  such  an  extent 
that  he  now  considers  himself  well.  The  electrocardiogram  is  of  further 
interest  because  it  gives  some  corroboration  of  the  clinical  findings : 
negative  T  in  L  I  and  an  abnormally  wide  R  deviation  in  L  I  and  III, 
presumed  evidences  of  myocarditis  (Chapter  IV) ;  the  positive  R  I  and 
negative  R  II  and  R  III  also  confirm  the  clinical  and  orthodiascopic 
findings  of  a  markedly  hypertrophic  left  ventricle. 

Electrocardiograms  of  ventricular  extrasystoles  vary  considerably 
from  normal  complexes  because  their  course  in  the  heart  (Fig.  38,  J,  K)  is 
quite  different  from  that  followed  by  the  normal  excitation  wave.  The 
extrasystoles  may  originate  in  either  ventricle.  There  is  experimental 
evidence  that  extrasystoles  arising  from  the  various  areas  of  the  ven- 
tricular musculature  —  so-called  ectopic  foci  (Lewis)  —  conform  to 
definite  electrocardiographic  types.     By  analogy,  it  is  possible  to  deter- 


72 


CLINICAL   CARDIOLOGY 


mine  in  the  human  being  the  abnormally  excitable  areas  in  the  ventricle, 
from  variations  in  the  form  of  the  atypical  electrocardiograms  (Fig.  154). 


R.N/ 


U.V. 


OASE. 


IT -J. APEX 


Fig.   154.  —  Schematic  view  of'  types  of  ventricular  extrasystole  arising  from  various 
ectopic  foci,  showing  the  direction  of  the  corresponding  R  deviations. 
R.  V  =  right  ventricle.  L.  V  =  left  ventricle. 


However,  one  must  remember  that  the  abnormal  path  followed  by 
extrasystoles  need  not  necessarily  indicate  a  corresponding  abnormal 
ventricular  focus  as  its  starting  point. 

Though  studies  of  the  various  forms  of  ventricular  extrasystoles  are 
of  considerable  interest  and  importance,  there  is  at  present  no  correla- 
tion, except  in  isolated  cases,  between  the  different  types  and  the  clinical 
condition.  It  is  to  be  noted  that  the  P  deviation  is  usually  not  visible 
because  it  is  lost  in  the  larger  ventricular  complex ;  occasionally,  how- 
ever, it  appears  at  such  time 
that  it  distinctly  notches  the 
R  wave. 

A  schematic  view  of  the 
usual  ectopic  foci  and  their 
corresponding  electrocardio- 
graphic types  is  given  in  Fig. 
154;  it  shows  the  direction 
of  the  R  and  T  deviations 
in  the  L  I  and  II.  These 
types  are  also  illustrated  by 
examples  of  ventricular  extra- 
systoles derived  from  human 
beings  (Figs.  155,  156,  157). 
That  there  are  intermediate 
types  coming  from  inter- 
mediate ectopic  foci  one  may 
assume  from  certain  rare  cases  of  ventricular  extrasystoles  with  heart 
block  showing  gradual  and  regularly  varying  abnormal  complexes  (Fig. 


Fig.  155.  —  Ventricular  extrasystole  (V.  Ex.) 
from  right  ventricle  near  the  base.  (Courtesy 
of  Dr.  A.  E.  Cohn.) 


THE   ARRHYTHMIAS 


73 


158).     It  is  as  if  the  abnormal  excitation  had  affected,  ladderwise  and 

in  progression,  various  successive  areas  of  the  ventricular  musculature. 

Instances  of  regularly  recurring  extrasystoles  (coupled  rhythm)  are 


I 


Fig.  156.  —  Ventricular  extrasystole 
(V.  Ex.)  from  left  ventricle  near  the 
base.     (Courtesy  of  Dr.  A.  E.  Colin.) 


t  ^  Jf^: 

WfJ 

iPffffft 

JS'll"' 

f  f^MBBjjjilHi 

0K**» 

§if|i§jM 

J 

MlHrlr  \T 

Mil 

mh 

i 

111 

-lUiHjHml'll 

■ 

I'll!! 

1 

il  111  i'i  iill'i  '1 

||i 

sffiffs 

WrTO+ffroffH-l- :  ff :  ] 

Fig.  157.  —  Ventricular  extrasystole 
(V.  Ex.)  from  wall  of  left  ventricle. 
(Courtesy  of  Dr.  A.  E.  Colin.) 


M 


-o  o 
>>  . 


-  a; 


El    0 

a>  en 
>  a) 


9"S 

O   d 

a 


given  in  Figs.  159,  159.4,  1595.  Occasionally  several  originate  from 
the  same  ectopic  focus  (Fig.  160),  producing  short  runs  of  paroxysmal 
tachycardia  of  ventricular  origin. 


74 


CLINICAL  CARDIOLOGY 


B  III.    Automatic  Ventricular  Activity  —  Ventricular  Escape 

This  rare  type  consists  in  the  sudden  '  escape  '  of  the  ventricle  from 
auricular  control,  and  results  in  ventricular  automatism  or  independent 
activity.     In  a  few  cases  that  had  been  previously  described  there  was 

marked  retardation 
of  the  auricular, 
and,  in  most  in- 
stances, of  the  ven- 
tricular rate.  In 
the  case  which  I 
observed  there  was 
never  any  marked 
pulse  retardation 
(Fig.  161) ;  the 
lowest  rate  was  55 
per  minute  and  the 
auricular  speed  was 
not  abnormally 
slow.  Its  etiology 
will  be  discussed  in 
a  later  chapter 
(Chapter  VIII). 

When  auricles 
and  ventricles  beat 
at  such  rates  that 
their  waves  and 
deflections  in  the 
tracings  are  regu- 
larly superimposed, 
their  origin  in  or  near  the  auriculo-ventricular  node  has  sometimes 
been  assumed;  these  are  called  nodal  extrasystoles  (q.v.).  Such  si- 
multaneous action  is  seen  in  parts  of  the  electrocardiogram  of  the  case 
of  "ventricular  escape"  (Fig.  162,  X,  Plate  XIV),  but  it  apparently 
depends  on  transient  identical  auricular  and  ventricular  speeds.  For, 
as  the  latter  vary,  varying  a-c  and  c-a  (Fig.  161)  or  P-R  and  R-P 
intervals  (Fig.  162,  Plate  XIV)  soon  occur.  Besides,  nodal  beats  are 
usually  either  regularly  interpolated  in  the  normal  rhythm,  or,  when 
premature,  are  followed  after  longer  or  shorter  compensatory  pauses 
by  the  normal  dominant  beat. 

Such  assumptions  of  nodal  extrasystoles  are  therefore  not  warranted,  I 
believe,  by  the  electrocardiograms  here  shown,  all  of  whose  complexes  are  alike. 
Backward  conduction  (q.v.)  from  ventricle  to  auricle,  a  rare  reversal  of  the 
cardiac  mechanism,  also  requires  consideration  as  a  possible  explanation.  In 
the  case  there  described,  the  rhythm,  when  established  showed  a  definite  ven- 
triculo-auricular  conduction  time  similar  to  the  normal,  and  was  accompanied 
by  marked  ventricular  slowing.     This  conception  if  applied  to  my  case  would 


Fig.  159.  —  Regularly  recurring  ventricular  extrasystoles 
(V.  Ex.)  : — coupled  rhythm  (pulsus  bigeminus).  (Cour- 
tesy of  Dr.  A.  E.  Cohn.) 


PLATE  XIV 


_^X ,*, — .       »« ! ! ! — . . 


Fig.  162.  —  Ventricular  escape.  Sections  of  a  continuous  tracing.  At  X  the  ventricle 
"escapes"  from  auricular  control  and  beats  independently  at  such  rate  that  auricle  and 
ventricle  occasionally  contract  synchronously  (superposition  of  P  and  R  waves).  The 
rhythm  is  sequential  in  the  other  parts  of  the  tracing. 


•  ♦L 

i 

H  ■- 

W 

R 

1 — 

7 

:- 

. 

- 

_1  . 

■_ 

1 

■ 

' 

f: 

-- 

■     l 

~ 

Fig.    169. — LI.      True   bradycardia.      The   auricles  and  ventricles  beat  sequentially. 

The  rate  is  50  per  minute. 


Fig.  183.  —  Prolonged  conduction  time.      P  —  R  =  .3  second. 


THE   ARRHYTHMIAS 


75 


hi 


7 


76  CLINICAL  CARDIOLOGY 

necessarily  also  assume  that  the  "reversed  mechanism  "  suddenly  and  irregularly 
ceased  from  time  to  time  in  those  parts  of  the  tracing  which  do  not  show  a 
"retrograde  conduction  time"  (c-a  or  R-P  intervals)  of  less  than  one  fifth 
second,  and  that,  frequently,  isolated  beats  were  retrograde.  This  hypothesis 
is  highly  improbable  and  is  not  supported  by  the  electrocardiogram.  Rihl  de- 
scribes a  case  of  occasional  automatic  ventricular  action  produced  by  vagal 
pressure.  Lewis  reports  a  case  of  rheumatic  mitral  stenosis  with  decompensa- 
tion ;  digitalis  had  been  given  with  resulting  ventricular  automaticity  ("  ven- 
tricular escape,"  Lewis).  Gallavardin,  Dufourt,  and  Petzetakis  describe  three 
cases  with  slow  pulses  (in  one  case  the  rate  was  36  per  minute)  in  which  there 
was  no  clinical  evidence  of  organic  cardiovascular  disease.  In  two,  numerous 
polygraph!  c  and  electrocardiographic  tracings  showed  the  occurrence  of  ven- 
tricular automatism  ;  in  all  three,  it  was  readily  evoked  by  ocular  and  vagus 
pressure,  and  by  atropin  injection.  The  writers  suggest  two  causes  for  the 
phenomena :  relative  retardation  of  the  auricular  as  compared  with  the  idio- 
ventricular rate,  or  acceleration  of  the  latter  beyond  the  former.  Two  of 
their  cases  had  very  slow  auricular  rates  occurring  either  spontaneously  or 
induced  by  the  methods  described ;  the  third  showed  no  auricular  retardation 
on  vagus  or  ocular  pressure,  or  after  atropin  injection.  The  arrhythmia  in  the 
first  two  cases  was  apparently  due  to  relatively  increased  idioventricular  rapidity 
beyond  that  of  the  sinus.  Except  for  a  very  slight  change  in  the  complexes 
of  the  automatic  ventricular  beats  in  two  of  the  cases  —  the  absence  of  a  very 
small  S  wave  —  all  of  the  complexes  are  identical.  In  digitalis  poisoning, 
Cohn  and  Fraser  have  occasionally  found  either  identical  auricular  and  ven- 
tricular speeds,  or  ventricles  beating  more  rapidly  than  auricles,  with  ven- 
tricular escape.  In  the  case  I  report  there  was  at  no  time  any  marked  pulse 
retardation  —  the  lowest  rate  was  55  —  nor  was  there  any  evidence  of  auric- 
ular slowing,  although  there  was,  at  the  periods  of  ventricular  automatism, 
some  slight  difference  between  auricular  and  ventricular  rapidity.  Except  for 
occasional  somewhat  slower  beats,  the  idioventricular  and  normal  ventricular 
rates  were  approximately  the  same.  Slight  sinus  arrhythmia  was  sometimes 
present,  but  was  not  more  marked  than  is  frequently  found  as  a  physiological 
phenomenon. 

B  IV.     Paroxysmal  Tachycardia  of  Ventricular  Origin 

As  with  the  auricular,  paroxysmal  tachycardia  of  ventricular  type 
is  marked  by  a  rapid  succession  of  ventricular  extrasystoles  (Fig.  160). 
This  type  of  irregularity  is  rare.  A  paroxysm  usually  comprises  from 
8  to  10  premature  contractions;  very  exceptionally,  there  may  be  as 
many  as  25  or  30. 

As  distinguished  from  paroxysmal  tachycardia  of  auricular  origin, 
the  runs  of  extrasystoles  in  the  ventricular  type  are  short ;  on  ausculta- 
tion, the  strong  "  thumps  "  indicating  extrasystoles  are  usually  quite 
evident. 

B  V.     Ventricular  Incoordination 

(1)  Ventricular  Fibrillation,  similar  to  the  incoordination  of  auricu- 
lar fibrillation,  is  due  to  incoordinate  ventricular  activity.  It  has  only 
very  rarely  been  studied  electrocardiographically  in  the  human  being. 
When  it  occurs,  so  far  as  we  now  know,  it  is  followed  by  death  within  a 
very  few  minutes.  The  reason  for  this  is  that  the  inchoate  ventricular 
contractions  have  no  propulsive  effect  upon  the  blood  in  the  ventric- 
ular chambers. 


THE   ARRHYTHMIAS 


77 


Branch-bundle  Lesions.  —  The  simplest  type  of  ventricular  inco- 
ordination consists  of  asynchronous  ventricular  contraction  from  lesions 
of  the  main  branches  of  the  auriculo-ventricular  bundle.  Such  lesions 
may  be  permanent  or  transitory.  In  these  lesions,  the  impulses  orig- 
inate in  the  A-V  bundle  before  its  bifurcation,  and  follow  the  un- 
blocked branch  in  the  ventricle  (Fig.  38,  II,  I).  Experimental  and 
clinical  examinations  have  shown  that  branch-bundle  lesions  produce 
characteristic  electrocardiograms.  Microscopic  sections  of  post-mortem 
specimens  have 
corroborated  and 
confirmed  the  elec- 
trocardiographic 
evidence  in  a  few 
instances. 

Since  the  excita- 
tion wave  travels 
along  the  healthy 
branch  and  excites 
the  corresponding 
ventricle  to  con- 
traction, the  elec- 
trocardiogram in 
the  various  leads 
shows  the  charac- 
teristics of  contrac- 
tion of  one  ventricle 
alone,  without  the 
counterbalanced 
contraction  of  the 
other.  Hence,  in  lesions  of  the  right  branch,  by  far  the  most  common, 
the  initial  deflections  show  left-sided  conduction.  The  deviations  are 
tall  and  positive  in  L  I,  and  tall  and  negative  in  L  III  (Fig.  164). 
The  opposite  is  the  case  in  the  left-sided  lesions  (right-sided  conduc- 
tion) (Fig.  163,  Plate  XIII).  A  further  characteristic  of  bundle 
lesions  is  the  abnormal  length  of  time  required  for  the  completion  of 
the  excitation  wave,  the  width  of  the  R  usually  being  about  .10  second. 
In  addition,  the  deviations  are  frequently  notched,  the  ventricular 
complex  usually  diphasic.  The  T  wave  is  commonly  deviated  in  a 
direction  opposite  to  that  of  its  accompanying  R  peak. 

The  electrocardiograms  of  cardiac  hypertrophy  are  somewhat  similar 
to  those  of  branch  lesions.  They  are  differentiated  by  a  narrower  R, 
the  lesser  amplitude  of  their  deflections,  the  direction  of  the  T  which 
is  the  same  as  that  of  the  R,  and  by  the  tri-  or  quadriphasic  character 
of  the  ventricular  complexes. 


Fig.  164.  —  Lesion  of  the  right  branch  of  the  conduction  sys- 
tem. Conduction  takes  place  along  the  left  branch.  The 
initial  deflections  are  tall  and  positive  in  L  I,  and  tall  and 
negative  in  L  III.     (Courtesy  of  Dr.  A.  E.  Cohn.) 


78 


CLINICAL  CARDIOLOGY 


C.     TRUE   BRADYCARDIA 

This  term  should  be  applied  only  to  types  of  slow,  regular  heart 
action  in  which  there  is  normal  conduction  time  from  auricle  to  ventricle, 
and  in  which  each  best  represents  a  sequential  auriculo-ventricular 
contraction.  Thus  defined,  it  has  its  proper  place  in  a  classification  of 
arrhythmias ;  otherwise,  when  loosely  used  in  the  sense  of  slow  pulse 
rate  (so-called  spurious  bradycardia),  it  takes  no  cognizance  of  auricular 
rhythm  or  of  auriculo-ventricular  conduction.     It  may  thus  haphazardly 


"»-f"T  ' 


$&&-%&?&**'■»"■• 


Fig.  166. 


Figs.  165-167. 


Fig.  167. 

True  bradycardia  from   patients  with  gastric  symptoms  and  normal 
hearts. 


include  such  divergent  cardiac  irregularities  as  auricular  fibrillation, 
extr asystoles,  and  heart  block  (q.v.).  It  is  difficult  to  fix  a  definite  rate 
as  typical  of  true  bradycardia.  Cardiac  and  pulse  rates  ranging  from 
60  to  65  per  minute  are  by  no  means  rare  in  normal  healthy  adults, 
especially  in  those  with  rather  marked  vasomotor  instability,  flushed 
hands  and  face,  sudden  irregular  pallor,  and  cold  and  moist  extremities. 
Examples  of  regular,  slow  heart  action  due  to  extracardial  causes  are 
given  in  Figs.  167,  168,  Fig.  169  (Plate  XIV).  An  instance  due  to 
salicylate  of  soda  is  shown  in  Fig.  168. 

In  the  electrocardiogram  of  true  bradycardia,  all  the  ventricular 
complexes  are  alike  ;  there  is  slow,  regular  heart  action.  Thus,  Fig.  169 
(Plate  XIV)  taken  from  a  young  epileptic  with  a  normal  cardiovascu- 
lar apparatus,  shows  regular  sequential  heart  beats  at  the  rate  of  50 
per  minute. 


THE   ARRHYTHMIAS  79 

Clinical  Recognition  of  True  Bradycardia.  —  The  rate  is  rarely 
below  40  per  minute ;  the  cardiovascular  apparatus  is  often  organically 
normal.  Since  in  true  bradycardia  the  auricles  and  ventricles  beat 
sequentially,  the  jugular  waves  (a  waves)  are  seen  to  precede  the  carotid 
pulsations  (c  waves).     True  bradycardia  must  be  differentiated  from  the 


$P     V         *■*   V 


RAoiAk  f?ATE       -  W-8      Pet*      M. 

Fig.  168.  —  True  bradycardia  caused  by  salicylate  of  soda. 

slow  heart  action  found  in  heart  block.  In  the  former,  the  jugular  pulsa- 
tions occur  with  the  same  frequency  as  the  carotid,  the  ventricular,  and 
the  pulse  beats  ;  in  the  latter,  they  occur  more  frequently.  The  jugular 
pulsations  may  be  rendered  more  prominent  by  having  the  patient  lie 
flat  and  by  inspection  of  the  right  side  of  the  neck.  By  holding  a  white 
card  in  the  space  between  the  jugular  and  carotid,  it  is  sometimes  possible 
to  reflect  the  jugular  pulsations  on  the  card  by  placing  the  patient  in 
the  proper  light. 

D.    ARRHYTHMIAS    PRODUCED    BY    ABNORMAL 

SEQUENCE  OF   CONTRACTION   OF  AURICLES 

AND   VENTRICLES 

This  sequence  may  be  disturbed  either  at  the  pacemaking  area 
(the  sino-auricular  node)  or  at  the  junctional  tissues  (the  atrioventric- 
ular node). 

D  I.     (1)  Sinus  Arrhythmia 

This  pulse  irregularity  is  produced  both  by  physiological  and  ab- 
normal influences  which  affect  the  sinus  region,  the  pacemaker  of  the 
heart.  Sinus  arrhythmia  of  the  physiological  respiratory  type  consists 
of  alternate  moderate  acceleration  and  retardation,  a  waxing  and  wan- 
ing of  the  pulse  rate,  corresponding  to  inspiration  and  expiration 
respectively.  The  arrhythmia  is  of  vagal  origin  and  is  ascribed  to 
differences  in  the  vagal  inhibitory  tone  from  phasic  respiratory  changes. 
It  is  a  physiological  phenomenon  in  children  (Figs.  170,  171)  and  young 
adults  (Fig.  172)  (the  "  youthful  irregularity  "  of  Mackenzie),  though 
it  is  by  no  means  uncommon  as  a  normal  variation  in  the  middle 
aged,  especially  upon  forced  deep  respiration.  Sinus  arrhythmias  due 
to  other  causes  are  also  illustrated  (Figs.  173-176). 


80 


CLINICAL   CARDIOLOGY 


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THE   ARRHYTHMIAS 


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CLINICAL  CARDIOLOGY 


In  the  electrocardiogram,  sinus  arrhythmia  is  recognized  by  varying 
lengths  of  the  pauses  between  the  beats  (Fig.  177) ;  there  is  no  difference 
in  any  of  the  complexes  unless  phasic  respiratory  variations  (Chapter 
IV)  are  present. 

Clinical  Recognition  of  Sinus  Arrhythmia.  —  The  physiological  type 
with  normal  pulse  rate  is  readily  diagnosed  because  it  wanes  and  waxes 
with  inspiration  and  expiration,  respectively.  The  pathological  types 
of  sinus  arrhythmia  do  not  usually  show  this  correlation.  The  clinical 
diagnosis  of  the  latter  is  then  made  by  the  comparatively  slow  pulse 
rate  with  irregularly  long  diastolic  pauses.  The  interventricular  interval 
may  be  sufficiently  long  to  block  out  an  entire  auriculo-ventricular  con- 
traction, thus  leading  to  sino-auricular  block  (q.v.).  The  distinction 
between  sinus  arrhythmia  of  the  non-respiratory  type  and  auricular 
fibrillation  with  slow  and  fairly  regular  ventricular  activity  depends 
upon  the  observation  of  the  jugular  pulsations.  In  the  former,  there 
are  regularly  recurring  jugular  waves  (a  waves)  which  precede  the 
carotid  pulsations;  in  the  latter  this  relationship  naturally  does  not 

■•  [  ■  .  i  i  ■  l  ■  i  I  i  ■■  I  i  i  i  I  I  I  I  I  i  I  l  ;  exist,  since  auric- 
^^^— ——~~~— ~—~—~— ~~~^t~ztz——~~~    ular   contractions 

are  absent. 

D  I.     (2)  Slno- 

atjriculak 

Block 

Occasionally 
abnormal  influ- 
ences affect  the 
vagus  or  its  end- 
ings in  the  sino- 
auricular  node  so 
that  an  entire  beat 
is  blocked. 

This  arrhyth- 
mia is  rare  in 
adults.  There  is 
stoppage  of  the 
entire  heart  (Fig. 
178:  Fig.  179, 
Plate  XV).  The 
pause  is  usually 
somewhat  less 
than    is   required 

for  two  normal  contractions ;  when  extreme,  the  pause  may  represent 
the  time  required  for  three,  or  even  four,  normal  beats.  I  have  seen 
two  cases  due  to  tabagism,  one  of  whom  had  an  organically  normal 


Fig.  178. 


Electrocardiogram  showing  sino-auricular  block 
(iS.^4.)  due  to  smoking. 


THE   ARRHYTHMIAS 


83 


heart;  the  other  patient  had  myocarditis  with  mild  decompensatory 
symptoms.  Figure  178  is  taken  from  one  of  these  patients.  In  ad- 
dition to  the  sino-auricular  block, 
there  is  moderate  tachycardia. 
This  double  effect  of  nicotine, 
moderate  tachycardia  and  sino- 
auricular  block,  was  probably  due  &.*. 
to  the  varying  action  of  the  poison 
upon  the  ganglionic  terminations 
of  the  vagus  and  sympathetic  (Fig. 
180).  In  the  other  case,  a  smoker 
with  myocarditis  and  decompen- 
sation, ventricular  extrasystoles 
(Fig.  179,  Plate  XV)  were  also 
present ;  sino-auricular  block  dis- 
appeared two  days  after  smoking 
was  stopped ;  the  extrasystoles 
ceased  some  days  later  when  com- 
pensation was  restored  by  the  use 
of  digitalis  and  theobromine  sodium 
salicylate. 


Fig.  180.  —  Diagram  showing  the  effect 
of  nicotine  upon  the  ganglionic  termi- 
nations of  the  vagus  and  accelerators. 
(Modified    from    Cushny'a    "Pharma- 


logy. 

') 

V 

=  vagus : 

A.C 

=  accelerator  fibers ; 

Ven 

=  ventricle ; 

A 

=  auricle ; 

M.S 

=  cardiac  musculature ; 

G.V 

=  ganglia   at   vagus   termina- 

tion ; 

G.S 

=  ganglia   at    termination    of 

sympathetic  nerve ; 

SP.C 

=  spinal  cord. 

D  I.     (3)  Blocked  Auriculae  Beat 

Ventricular  action  does  not  follow  the  blocked  auricular  impulse,  con- 
sequently there  is  a  quiescent  period  equivalent  to  two  beats  (Fig.  181). 

It  is  distinguished 
from  extrasystoles  by 
the  absence  of  the 
characteristic  small 
pulse  wave  and  of  the 
extrasystolic  heart 
sounds ;  from  sino- 
auricular  block,  only 
by  recognition  of  an 
auricular  jugular 
wave  in  the  former, 
and  its  absence  in 
the  latter. 


Fig.  181.  —  Blocked  auricular  beat.  Absence  of  ventricu- 
lar response,  also  showing  prolonged  conduction  time. 
(Courtesy  of  Dr.  A.  E.  Cohn.) 


D  II.     (1)  Prolonged  Conduction  Time 

This  represents  the  simplest  type  of  heart  block.  Various  factors 
cause  moderate  prolongation  of  the  impulse  from  auricle  to  ventricle, 
that  is,  of  the  P-R  time.  These  are  chiefly  digitalis  medication, 
myocarditis,  and  acute  endocarditis.  I  have  also  observed  lengthened 
conduction  in  several  patients  with  auricular  extrasystoles  of  functional 


84 


CLINICAL  CARDIOLOGY 


origin.     Cases   of   extreme  prolongation  of  the    P-R  time   up  to  or 
even  more  than  0.50  second  sometimes  occur.     For  example,  Fig.  182 

is   the   electrocar- 


Fig. 


diogram  of  a  male 
patient  aged  62, 
who  had  myocar- 
ditis and  nephritis ; 
at  the  time  that 
the  electrocardio- 
gram was  taken  he 
was  suffering  from  a  third  attack  of  severe  decompensation ;  dyspnoea, 
oedema  of  the  legs,  ascites.  He  died  later  with  uremic  symptoms. 
The  electrocardiogram  shows  a  ventricular  rate  of  37  per  minute  with  a 
conduction  time  of  0.8  second.  A  less  marked  instance  is  shown  in 
Fig.  183  (Plate  XIV). 


182.  —  Electrocardiogram  showing  very  slow  ventricular 
rate  (37  per  minute)  with  a  P-R  time  of  .8  second. 


D  II.     (2)  Shortened  Conduction  Time 

The  normal  P-R  interval  is  from  .16  to  .20  second.  This  interval 
—  the  conduction  time  from  auricle  to  ventricle  —  is  occasionally 
shortened  in  both  paroxysmal  and  simple  tachycardia ;  however,  rapid 
cardiac  activity  in  these  arrhythmias  occurs  mainly  at  the  expense  of 
diastole. 


D  II.     (3)  Backward  Conduction  from  Ventricle  to  Auricle 

This  exceedingly  rare  anomaly  is  exemplified  in  Fig.  184.  It  shows 
the  auricular  (P),  regularly  following  the  ventricular,  beat.  Backward 
conduction  was  also  corroborated  in  that  case  by  fluoroscopic  examina- 
tion.    The  patient,  a  laborer  of   51  suffering  from   diarrhea  for  one 


Fig.  184.  —  Electrocardiogram  showing  backward  conduction  from  ventricle  to  auricle. 
(From  Williams  and  James — "Reversal  of  the  Cardiac  Mechanism."  Heart,  1913-14, 
V,  109). 

year,  had  attacks  of  Stokes-Adams  syndrome.  The  cardiovascular 
system  was  apparently  normal  organically.  The  arrhythmia  persisted 
for  many  months  and  was  not  affected  by  atropin  injections.  Finally, 
the  rhythm  again  became  normal.  The  writers  ^  suggest  as  possible 
etiological  factors  abnormal  vagus  control  or  a  toxic  cause. 


THE   ARRHYTHMIAS 


85 


D  II.     (4)   (a)  Incomplete  Heart  Block 


In  its  simplest  type,  this  consists  in  the  absence 
response  to  auricular  impulses.  There  is  a  geometric 
auricular  and  ventricular  beats ; 
for  example,  the  ventricle  re- 
sponds to  every  second,  third,  or 
fourth  auricular  impulse.  Such 
cases  are  termed  incomplete  heart 
block  at  2 :  1,  3 :  1,  etc.  ratio  re- 
spectively (Figs.  185,  186).  The 
ventricle  and  pulse  beat  rhythmi- 
cally unless  disturbed  by  oc- 
casional premature  ventricular 
contractions  (Fig.  186,  c').  In 
other  types  oi  incomplete  block 
the  ventricular  response  varies 
irregularly  from  one  ratio  to 
another ;  the  ventricle,  for  exam- 
ple, answers  haphazardly  every 
second  or  third  or  fourth  auricu- 
lar impulse.  The  pulse  becomes 
correspondingly  irregular.  In 
both  incomplete  and  complete 
block,  the  auricles  beat  rhyth- 
mically at  approximately  normal 
speeds,  60  to  80  times  per  minute. 
In  incomplete  heart  block,  the 
ventricular  rate  is  considerably 
diminished ;  as  stated,  its  regu- 
larity depends  upon  the  auriculo- 
ventricular  ratio. 

D  II.     (4)  (b)  Complete 
Heart  Block 

This  is  said  to  exist  when 
there  is  no  relationship  between 
auricular  and  ventricular  speeds. 
The  ventricle  follows  its  own  in- 
herent rhythm  (Figs.  187-196). 
The  usual  inherent  (idioventricu- 
lar) rate  of  the  atrioventricular 
node  is  between  25  and  40  per 
minute.  Complete  heart  block 
represents    the    purest   type   of 


of  ventricular 
ratio  between 


86 


CLINICAL   CARDIOLOGY 


THE   ARRHYTHMIAS 


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CLINICAL   CARDIOLOGY 


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THE   ARRHYTHMIAS 


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90  CLINICAL   CARDIOLOGY 

regular  heart  action.  Polygraphically,  the  carotid  (c)  waves  are  iden- 
tified in  the  usual  manner.  Since  the  auricular  speed  varies  but 
slightly  if  at  all,  the  auricular  (a)  waves  are  recognized  by  their  oc- 
currence at  regularly  spaced  intervals  (Figs.  187,  188).  Because  of 
their  varying  rates,  the  a  and  c  waves  occasionally  fall  simultaneously 
with,  and  are  superimposed  into,  taller  or  broader  peaks  (Figs.  190, 
193).  Fig.  191  resembles  incomplete  block,  because  auricular  and 
ventricular  rates  temporarily  correspond.  Examination  of  longer  sec- 
tions, however,  show  that  this  ratio  is  accidental,  for,  with  slightly 
varying  auricular  and  ventricular  speeds,  there  is  at  first  closer  ap- 
proximation and  finally  superposition  of  the  a  and  c  waves  (Fig.  191 B). 
In  complete  heart  block,  auricular  activity  is  occasionally  abnormally 
rapid,  so  that  its  ratio  to  ventricular  beats  is  as  four  or  five  to  one. 
While  regular  rhythmic  activity  is  the  rule  in  complete  heart  block, 
there  are  exceptions ;  as,  for  instance,  slight  variations  in  the  ventricular 
rhythm  (Fig.  193).  The  regularity  may  also  be  disturbed  by  ventricular 
extrasystoles.  These  are  usually  single  (Fig.  194,  /).  The  pause  fol- 
lowing them  is  not  compensatory,  but  is  equal  in  length  to  a  rhythmic 
beat.  Very  rarely  such  extrasystoles  are  multiple  (Figs.  195  A  and  B, 
r',  r"). 

The  ease  illustrated  by  Fig.  195  was  originally  one  of  complete  heart  block 
with  a  rhythmic  ventricular  rate  of  35,  and  an  auricular  speed  of  72  per  minute, 
as  demonstrated  by  polygraphic  and  electrocardiographic  tracings.  The  auric- 
ular beats  could  be  plainly  heard  in  the  interventricular  pauses.  Through 
inadvertence  on  the  part  of  the  nurse,  digitalis  was  administered  for  several 
weeks  after  having  been  ordered  discontinued.  The  pulse  then  became  arrhyth- 
mic. The  auricular  beats  were  no  longer  heard.  '  Extrasystoles  '  {i.e.  ectopic 
beats),  most  of  which  were  frustrane,  were  heard  at  the  apex.  The  tracing  shows 
some  of  them  registered  in  both  radial  and  jugular  (Fig.  195  A,  B,  r',  c',  r",  c") ; 
others  in  the  jugular  only  (Fig.  195  A,  B,  c") ;  regularly  recurring  auricular  waves 
could  not  be  identified.  Digitalis  was  discontinued.  After  two  weeks,  the  orig- 
inal type  of  heart  block  was  present,  as  shown  by  electrocardiographic  tracings, 
and  the  auricular  beats  were  again  heard.  From  the  auscultatory  evidence,  from 
the  absence  of  auricular  waves  in  the  jugular,  and  from  the  fact  that  digitalis 
poisoning  sometimes  induces  auricular  fibrillation  and  'extrasystoles,'  it  seems 
probable  that  the  polygraphic  tracing  represents  heart  block,  auricular  fibrilla- 
tion, and  ectopic  beats  —  a  unique  instance  of  digitalis  poisoning  in  a  patient  with 
complete  heart  block. 

Another  rare  example  of  peculiar  disturbance  of  ventricular  rhythm  is  that 
represented  in  Fig.  196  A  and  B,  taken  from  a  patient  on  successive  days. 
Digitalis  had  not  been  given.  The  radial  tracing  showed  ventricular  ar- 
rhythmia due  to  abrupt  and  reciprocal  changes  from  faster  to  slower  rates.  The 
faster  rate  was  66;  the  slower,  47  per  minute.  The  auricular  speed  remained 
constant  at  55.  A  study  of  the  polygraphic  tracing  corresponding  to  the  faster 
beats  (included  in  the  brackets)  showed  an  extremely  long  conduction  time, 
the  a-c  interval  varying  from  .50  to  .55  second.  Occasionally  the  ventricle 
did  not  respond  but  contracted  at  the  idioventricular  rate  (complete  heart  block). 
This  condition  existed  for  one  week.  Thereafter  electrocardiograms  taken 
frequently  for  a  period  of  1|  years  always  showed  complete  block  (Fig.  179, 
Plate  XV),  the  auricular  speed  being  100  to  110,  the  ventricular  45  to  50  per 
minute.     The  block  was  uninfluenced  by  atropin  injections. 

Higher  rates  are  occasionally  encountered  in  heart  block.     For  ex- 
ample, in  one  of  my  cases,  the  ventricular  rate  was  at  one  time  as  high  as 


> 
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THE   ARRHYTHMIAS 


91 


77  per  minute  and  the  rhythm  slightly  irregular.  The  following  are  ex- 
amples of  heart  block  with  varying  auricular  and  ventricular  rates.  Fig- 
ure 197  (Plate  XV),  from  a  man  of  GO  with  myocarditis  and  aortitis, 
shows  complete  heart  block.  Figure  198  (Plate  XVI)  is  given  in  two 
parts  :  A,  illustrates  incomplete  block  with  a  2  :  1  rhythm  ;  B,  taken  a 
few  moments  later,  shows  complete  block.     In  section  A  the  block  only 


r~. — ~ ' — rr 


^"^1  IMIIHI|IWMI||||J: 


Fig.   197.  —  Complete  heart  block.     The  ventricular  rate  is  30 ;  the  auricular,  75  per 
minute.     (Courtesy  of  Dr.  A.  E.  Conn.) 


appears  incomplete  because  of  slightly  varying  auricular  and  ventricular 
speeds.  This  tracing  was  taken  from  a  young  man  who  had  peritoneal 
tuberculosis  with  irregular  fever  and  who,  except  for  the  arrhythmia, 
presented  no  sign  of  cardiac  disease.  The  lungs  were  normal.  The 
patient  had  been  in  the  habit  of  feeling  his  pulse  before  his  illness  and 
had  always  found  it  of  normal  rapidity,  that  is,  about  70  per  minute. 
The  peritoneal  tuberculosis  became  quiescent  following  laparotomy. 
The  heart  block  continued.  Atropin  was  injected  several  times  without 
influencing  the  block.  Its  only  effect  was  a  slight  transient  increase 
of  the  ventricular  rate.  The  patient  died  two  years  later  as  the  result 
of  an  accident.  A  necropsy  was  performed.  In  the  abdomen,  omental 
tuberculosis  was  found.  The  lungs  were  normal ;  there  were  no  en- 
larged glands  at  the  pulmonary  hilus.  On  careful  macroscopic  ex- 
amination, the  cardiac  valves  and  musculature  were  found  normal. 
Though  at  the  present  writing,  the  atrio-ventricular  conduction  system 
has  not  been  microscopically  examined,  there  was  no  evidence  of  any 
gross  lesion  at  the  site  of  the  bundle.  In  other  words,  there  was  no 
apparent  pathological  change  in  the  heart  itself  to  account  for  the 
block.  This  case  will  be  etiologically  discussed  in  another  place 
(Chapter  VIII). 

Clinical   Recognition  of   Heart   Block.  —  The   ventricular  rate  in 
complete  heart  block  is  usually  between  25  and  40,  although  rates  as 


92  CLINICAL   CARDIOLOGY 

low  as  8  per  minute  have  been  reported.  The  auricular  beats  are  often 
heard  in  the  apical  region  or  at  the  third  left  interspace  as  soft  faint 
distant  sounds,  interspersed  between  the  ventricular  contractions. 
Synchronous  with  the  sounds  of  the  auricular  contractions,  jugular 
pulsations  unaccompanied  by  carotid  beats  may  be  seen  in  the  neck. 
There  are  no  compensatory  pauses  in  the  regular  ventricular  action  of 
heart  block,  thus  distinguishing  this  arrhythmia  from  extrasystoles. 
Incomplete  heart  block  with  changing  ventricular  ratios,  for  example 
from  2:1  to  3:1,  requires  differentiation  from  sino-auricular  block ; 
this  distinction  is  based  chiefly  upon  the  auricular  contractions  which  are 
present  and  sometimes  audible  in  the  first  type  of  arrhythmia,  and 
upon  the  absence  of  auricular  beats,  visible  or  audible,  in  sino-auricu- 
lar block.  It  is  sometimes  possible  to  diagnose  complete  heart  block 
merely  from  observation  of  the  pulsations  in  the  neck.  Prominent 
pulsations  indicative  of  the  simultaneous  contraction  of  auricle  and 
ventricle  (a  +  c  wave),  or  auricular  with  ventricular  filling  wave 
(a  +  v  wave)  can  then  be  observed.  Similar  large  jugular  waves 
sometimes  seen  with  extrasystoles  (cV,  a'c'  or  c'a  waves)  are  differen- 
tiated from  those  in  heart  block  by  the  slow  ventricular  rate  of  the 
latter. 

Pulse  Alternation  —  Pulsus  Alternans.  —  This  is  a  disturbance,  not 
of  rhythm,  but  of  strength  of  the  ventricular  contractions,  and  therefore 
of  the  pulse  beats ;  strong  beats  regularly  alternate  with  weaker  ones. 
Alternation  of  the  pulse  is  often  not  sufficiently  marked  to  be  detected 
by  palpation  (Figs.  199-200),  hence  the  importance  of  radial  tracings 
for  its  diagnosis.  It  occurs  in  tachycardia,  especially  when  paroxysmal, 
and  results  then  directly  from  the  ventricular  acceleration.  Alterna- 
tion is  also  fairly  common  after  extrasystoles  (Figs.  200-201). 

This  condition  is  usually  found  in  patients  with  dangerously 
weakened  myocardium  and  is  commonly  regarded  as  of  grave  prognostic 
import.  However,  alternation  is  occasionally  found  in  patients  with 
normal  hearts,  or  as  the  result  of  digitalis  medication.  The  question 
of  the  mechanism  of  alternation  is  the  subject  of  many  conflicting 
opinions  and  theories.  The  condition  has  been  ascribed  to  disturbance 
of  the  function  of  contractility ;  to  the  fact  that  not  all  the  ventricular 
fibers  contract  with  the  smaller  beat;  or  because  the  systoles  of  the 
stronger  are  of  longer  duration  than  those  of  the  weaker  beats,  thus 
encroaching  upon  the  rest  period  of  the  latter.  Electrocardiographic 
tracings  of  patients  with  alternation  have  partly  upset  some  of  these 
hypotheses.  For  example,  there  is  no  evidence  that  varying  amounts 
of  ventricular  musculature  are  involved  or  that  the  path  followed  by  the 
weaker  differs  from  that  of  the  stronger  contractions  ;  nor  is  there  any  dif- 
ference in  duration  of  their  contraction  times.  Einthoven  suggested  an 
explanation  similar  to  that  involved  in  the  irregular  pulse  excursions 
of  auricular  fibrillation,  namely,  that  the  increased  blood  pressure  of 


THE   ARRHYTHMIAS 


93 


94  CLINICAL   CARDIOLOGY 

the  stronger  contractions  acting  upon  a  weakened  myocardium  prevents 
the  heart  from  properly  emptying  itself  at  the  next  systole,  and  con- 
sequently produces  a  smaller  pulse.  This  theory  puts  the  explanation 
a  step  nearer,  but  scarcely  explains  the  rhythmic  alternating  regularity 
in  pulse  pressure. 

Pulsus  Paradoxus.  —  This  irregularity  is  indicated  by  a  gradual 
waning  and  waxing  in  the  strength  of  the  pulse  beat  with  respiration, 
but  without  any  change  of  rhythm.  It  has  been  regarded  as  charac- 
teristic of  pericarditis  with  effusion.  I  have  found  it  especially  in  cases 
of  severe  myocardial  insufficiency.  Occasionally  the  pulse  becomes  so 
weak  and  small  as  to  be  scarcely  perceptible  on  palpation. 


REFERENCES 
Chapter  VII 

Cohn,  A.  E.,  and  Fraser,  J.  R. :   Certain  Effects  of  Digitalis  on  the  Heart ;   In- 
ternational Medical  Congress,  1913,  Section  6,  Part  2,  258. 
Cushny,  A.  R. :  Pharmacology  and  Therapeutics ;  Edition  1913. 
Dresbach,  M.,  and  Munford,  S.  A. :   Interpolated  Extrasystoles ;   Heart,  1913- 

1914,  V,  197. 

Einthoven,  W.,  and  Korteweg,  A.  J. :  On  the  Variability  of  the  Size  of  the 
Pulse  in  Cases  of  Auricular  Fibrillation  ;   Heart,  1915-1916,  VI,  107. 

Fulton,  F.  T. :  Auricular  Flutter ;  Archives  of  Internal  Medicine,  1913,  XII, 
475. 

Gallavardin,  L.,  Dufourt,  P.,  et  Petzetakis :  Automatisme  Ventriculaire  Inter- 
mittent; Archives  des  Maladies  du  Cceur,  1914,  1. 

Gaskell,  W.  H. :  On  Innervation  of  the  Heart,  with  Special  Reference  to  the  In- 
nervation of  the  Heart  of  the  Tortoise  ;  Journal  of  Plxysiologj7,  1883,  IV,  43. 

Griffith,  T.  W.,  and  Cohn,  A.  E. :  Remarks  on  the  Study  of  a  Case  showing 
Greatly  Lengthened  A-C  Interval,  etc. ;  Quarterly  Journal  of  Medicine, 
1910,  III,  126. 

Halsey,  R. :   A  Case  of  Ventricular  Fibrillation ;   Heart,  1915,  VI,  67. 

Hart,  T.  S. :    Abnormalities  of  Myocardial  Function ;    Archives  of  Diagnosis, 

1915,  26. 

Hart,  T.  S. :  Paroxysmal  Tachycardia;  Heart,  1912-1913,  IV,  128. 

Hertz,  A.  F.,  and  Goodhart,  G.  W. :    The  Speed  Limit  of  the  Human  Heart ; 

Quarterly  Journal  of  Medicine,  1908-1909,  II,  213. 
Hering,  H.  E. :   Die  nomotope  und  heterope  Automatie  des  Herzens;   Congress 

fur  Innere  Medizin,  1911,  XXVIII. 
Hirschfelder,  A.   D. :    Simple  Methods  in  Cardiac  Diagnosis;    The  Virginia 

Medical  Semi-Monthly,  1913,  XVIII,  573. 
Jolly,  W.  A.,  and  Ritchie,  W.  T. :   Auricular  Flutter  and  Fibrillation ;    Heart, 

1910-1911,  II,  177. 
Levine,  S.  A. :    Observations  on  Sino-auricular  Heart  Block ;    Archives  of  In- 
ternal Medicine,  1916,  XVII,  153. 
Levy,  A.  G. :    The  Genesis  of  Ventricular  Extrasystoles  under  Chloroform ; 

Heart,  1913-1914,  V,  299. 
Lewis,  T. :   Clinical  Electrocardiography ;   Edition  1913. 
Lewis,  T. :   Auricular  Flutter;    Heart,  1912-1913,  IV,  171. 
Lewis,  T. :   Pathology  of  the  Heart  Function ;   Lancet,  October  10,  1914,  883. 
Lewis,  T. :   Irregular  Action  of  the  Heart  in  Mitral  Stenosis ;   Quarterly  Journal 

of  Medicine,  1908-1909,  II,  356. 
Mackenzie,  J. :   Diseases  of  the  Heart ;   3d  Edition,  238. 
Neuhof,  S. :    Transient  Auricular  Flutter  Accompanying  Acute   Endo-pericar- 

ditis  ;  New  York  Medical  Record,  December  11,  1915. 


THE  ARRHYTHMIAS  95 

Neuhof,  S. :  Auricular  Flutter  Occurring  during  Rheumatic  Endocarditis  ;  New 
York  Medical  Record,  1914,  LXXXVI,  63. 

Neuhof,  S.  :  Independent  Ventricular  Activity  Occurring  during  Acute  Artic- 
ular Rheumatism  ;  Archives  of  Internal  Medicine,  1915,  XV,  169. 

Neuhof,  S. :  Sino-aurieular  Block  due  to  Tobacco  Poisoning ;  Archives  of 
Internal  Medicine,  1916,  XVII,  659. 

Neuhof,  S. :  Independent  Ventricular  Activity ;  Archives  of  Internal  Medicine 
1915,  XV,  169. 

Neuhof,  S. :  Complete  Heart  Block  with  Rapid  Irregular  Ventricular  Activ- 
ity;  American  Journal  of  Medical  Sciences,  1913,  CXLV,  513. 

Parkinson,  J.,  and  Mathias,  H.  H.  :  Tachycardia  of  Auricular  Origin  and  Flutter 
with  Phasic  Variations  in  Auricular  Rate  and  in  Conduction ;  Heart, 
1915,  VI,  27. 

Rihl,  J. :  Klinische  Beobachtungen  ueber  atrioventrikulaere  Automatie  mit 
Bradykardie ;  Zeitschrift  fuer  Expt.  Pathologie  und  Therapie,  1911,  IX, 
496. 

Ritchie,  W.  T. :  Further  Observations  of  Auricular  Flutter ;  Quarterly  Journal 
of  Medicine,  1913-1914,  VII,  1. 

Ritchie,  W.  T. :  Auricular  Flutter. 

Rothberger,  C.  J.,  und  Winterberg,  H. :  Studien  ueber  die  Bestimmung  des  Aus- 
gangpunktes  ventrikulaerer  Extrasystolen  mit  Hilfe  des  Elektrokardio- 
gramms;  Archiv  fuer  die  ges.  Physiologie,  1913,  CLIV,  571. 

Rothberger,  C.  J.,  und  Winterberg,  H. :  Ueber  die  Entstehung  und  die  Ursache 
des  Herzflimmerns ;  Zentralblatt  fuer  Herz  und  Gefaesskrankheiten  ; 
1914,  VI,  453. 

Sutherland,  G.  A. :  Auricular  Flutter  with  Acute  Rheumatic  Carditis ;  British 
Journal  of  Diseases  of  Children,  1914,  XI,  337. 

Thayer,  W.  S. :  Adams-Stokes  Syndrome ;  Persistent  Bradycardia  .  .  .  Re- 
markable Prolongation  of  the  As-Vs  Interval ;  Archives  of  Internal  Medi- 
cine, 1916,  XVII,  13. 

Thayer,  W.  S.,  and  Peabody,  F.  W. :  A  Study  of  Two  Cases  of  Adams-Stokes 
Syndrome  with  Heart  Block;  Archives  of  Internal  Medicine,  1911,  VII, 
289. 

Williams,  H.  B.,  and  James,  H. :  Reversal  of  the  Cardiac  Mechanism ;  Heart, 
1913-1914,  V,  109. 


CHAPTER  VIII 
THE   ARRHYTHMIAS  —  THEIR   ETIOLOGY   AND   THERAPY 

At  the  outset  it  is  important  to  emphasize  that,  although  certain 
types  of  arrhythmias  may  be  associated  with  various  pathological  en- 
tities, almost  any  irregularity  may  be  the  result  of  non-organic,  neuro- 
genic, so-called  '  functional '  causes.  From  the  standpoint  of  etiology, 
therefore,  it  is  necessary  first  to  discover,  if  possible,  whether  the 
arrhythmia  is  of  functional  or  of  organic  origin.  Therapy  will  be  only 
briefly  touched  upon  here ;  fuller  details  will  be  found  in  the  chapter  on 
Circulatory  Remedies  (Chapter  XVI). 

Sinus  Arrhythmia 

As  a  physiological  phenomenon,  sinus  arrhythmia  is  quite  common 
not  only  in  children  and  young  adults  but  in  the  middle-aged.  It  is, 
however,  not  confined  to  normal  hearts.  I  have  found  the  condition 
in  young  individuals  suffering  from  aortal  or  mitral  disease.  The  hearts 
of  these  patients  were  compensated ;  they  had  not  received  digitalis. 
Possibly  this  arrhythmia  in  patients  with  heart  disease  can  be  regarded 
as  a  favorable  sign,  since  it  is  an  evidence  of  physiological  vagal  control. 
It  is  also  frequent  as  a  phenomenon  after  febrile  respiratory  catarrh 
terminating  by  critical  defervescence.  The  arrhythmia  is  then  regarded 
by  many  observers  as  the  result  of  toxic  or  infectious  myocarditis.  Its 
innocent  nature,  however,  is  proven  by  its  disappearance  within  a  few 
days,  and  by  the  absence  of  all  signs  of  cardiac  disease.  Sinus  slowing 
is  sometimes  a  purely  pathological  occurrence ;  it  then  bears  no 
relation  to  breathing.  For  example,  it  occurs  in  severe  secondary 
anemia  following  sharp  hemorrhage.  I  have  observed  two  such  cases. 
In  both  the  sensorium  was  clear  and  the  arrhythmia  gradually  disap- 
peared with  improvement  in  the  anemia.  In  such  instances,  I  believe 
sinus  arrhythmia  due  to  nutritional  changes  in  the  sino-auricular  node, 
or  to  increased  vagus  inhibition  on  the  part  of  the  cardio-inhibitory 
center.  In  another  case,  an  adult  whose  heart  at  necropsy  showed 
marked  presenile  cardiosclerosis  involving  the  endocardium,  mitral 
valves,  aorta  and  the  coronaries,  the  pulse  ranged  between  50  and  60 

96 


THE   ARRHYTHMIAS  97 

during  the  last  year  of  life.  Polygraphic  tracings  showed  sinus  ar- 
rhythmia. Microscopical  examination  of  the  sino-auricular  node  was 
not  made ;  sclerotic  changes  in  that  region  may  have  been  the  etiological 
factor. 

Physiological  sinus  arrhythmia,  or  sinus  arrhythmia  encountered  in 
febrile  crises,  requires  no  medication.  When  due  to  the  other  etiological 
factors  above  mentioned,  treatment  should  be  directed  to  them  rather 
than  to  the  arrhythmia  itself. 

SlNO-AURICULAR   BLOCK 

This  is  usually  the  result  of  digitalis  poisoning.  It  has  also  been 
produced  by  pressure  over  the  vagus  in  the  neck,  by  pressure  upon  the 
eyeballs  (oculo-cardiac  reflex)  in  human  beings  and  by  various  experi- 
mental procedures  in  animals.  It  is  occasionally  the  result  of  tobacco 
poisoning  (Fig.  178,  Fig.  179,  Plate  XV).  Otherwise  it  is  exceedingly 
rare  as  a  clinical  phenomenon.  The  condition  in  itself  requires  no 
medication  unless  accompanied  by  dizziness ;  atropin  sulphate  is  then 
sometimes  of  value. 

EXTRASYSTOLES 

Though  there  are  exceptions,  auricular  extrasystoles  are  usually 
of  functional  origin;  the  ventricular  may  be  functional  or  organic. 
When  organic,  auricular  or  ventricular  extrasystoles  may  mark  the  be- 
ginning of  decompensation  and  then  remain  as  permanent  arrhythmias. 
In  acute  heart  failure,  they  are  sometimes  the  forerunners  of  a  fatal 
termination.  The  onset  or  exacerbations  of  acute  endo-  or  pericarditis 
may  be  accompanied  by  extrasystoles.  We  do  not  know  in  what  manner 
organic  lesions  increase  ventricular  excitability  and  thus  produce  pre- 
mature contractions,  although  it  seems  probable  that  impaired  cardiac 
nutrition  plays  an  important  role  when  severe  cardiac  disease  is  present. 

When  extrasystoles  are  found  in  cardiac  failure,  the  treatment  of 
the  latter  is  the  prime  consideration  (Chapter  XVI).  When  caused 
by  endo-  or  pericarditis,  the  therapy  consists  mainly  of  salicylates  in 
large  doses.     Occasionally  the  addition  of  bromides  is  of  value. 

Functional  Extrasystoles  of  Extracardiac  Origin.  —  Cerebellar  and 
cerebral  conditions  which  exert  pressure  directly  or  indirectly  upon 
the  cardio-inhibitory  center  can  cause  premature  contractions.  These 
factors  apparently  act  by  direct  excitation  of  the  vagus  center.  Thus, 
a  patient  with  cerebellar  tumor  and  normal  circulatory  apparatus  had 
occasional  extrasystoles  during  the  last  few  months  of  life.  That  they 
were  due  to  pressure  was  demonstrated  at  operation  for  removal  of  the 
tumor.  The  latter  was  deeply  seated,  each  attempt  at  its  removal 
being  acompanied  by  premature  contractions.  Acute  gastric  disease 
with  vago-excitative  characteristics,  less  often  intestinal  disease,  are 
occasionally  accompanied  by  extrasystoles,  usually  auricular  in  type. 


98  CLINICAL  CARDIOLOGY 

Their  etiology  has  been  variously  explained.  The  usual  theory  is  that, 
after  a  meal,  the  distended  stomach  presses  the  diaphragm  against  the 
heart,  thus  embarrassing  circulation.  Another  reason  given  is  the 
action  of  absorbed  toxic  products  upon  the  neurogenic  cardiac  control. 
In  the  majority  of  cases  that  have  come  under  my  observation,  the  extra- 
systoles  occurred  most  frequently  when  the  stomach  was  empty.  Several 
of  these  patients,  fluoroscoped  after  a  bismuth  meal,  showed  no  gastric 
distention  or  other  evidence  of  abnormal  pressure  against  the  diaphragm ; 
in  fact,  their  stomachs  were  contracted  and  hypermotility  was  present. 
These  observations  nullify,  I  believe,  the  commonly  advanced  theories. 
The  intimate  physiological  relationship  between  the  nerves  of  the  stom- 
ach and  those  of  the  heart  lead  me  to  believe  that  extrasystoles  accom- 
panying gastric  disturbances  are  probably  caused  by  reflex  excitation 
of  the  cardiac  nerves.     The  path  of  the  reflex  arc  is  not  clear. 

Acute  inflammation  of  the  gall-bladder  and  bile  ducts,  with  or  with- 
out gastric  symptoms,  may  also  be  accompanied  by  premature  contrac- 
tions. Though  the  theory  is  based  upon  insufficient  data,  toxemia  has 
been  assumed  as  the  etiological  factor  for  the  extrasystoles.  The  ar- 
rhythmia is  often  present  very  early  in  the  disease,  when  extensive  toxic 
absorption  appears  improbable.  Similar  to  the  views  expressed  with 
reference  to  extrasystoles  in  gastric  disturbances,  I  believe  that  most 
cases  occurring  in  gall-bladder  disease  are  caused  by  reflex  excitation 
of  the  neurogenic  control  of  the  heart,  though  at  present  the  centripetal 
nerve-path  involved  is  unknown. 

Peritonitis  is  another  disease  in  which  premature  contractions  may 
occur.  One  case  of  appendicitis,  followed  by  general  peritonitis  and 
death,  in  an  elderly  individual  with  cardiosclerosis,  had  ventricular 
extrasystoles  at  the  onset  of  the  attack ;  during  the  last  few  days  of  life, 
auricular  fibrillation  was  present.  It  was  impossible  to  decipher  the 
varying  roles  played  by  toxemia  and  reflex  nerve  excitation  in  the 
production  of  these  arrhythmias ;  in  this  case  I  believe  both  were  factors. 

The  onset  and  crisis  of  acute  catarrhal  febrile  affections  are  fre- 
quently marked  by  premature  contractions.  The  latter  are  generally 
regarded  as  evidence  of  toxic  myocarditis.  For  several  reasons  this  re- 
lationship seems  doubtful  to  me.  Most  of  the  cases  I  have  observed  were 
not  toxic :  the  extrasystoles  occurred  with  mild  grippe  and  tonsillar 
affections  in  patients  who  scarcely  felt  ill.  The  arrhythmia  was  found 
at  the  crisis  or  immediately  thereafter  when  the  severe  symptoms 
had  disappeared.  There  were  no  circulatory  symptoms.  On  clinical 
grounds,  therefore,  it  seems  probable  to  me  that  these  extrasystoles  are 
due  to  abnormal  products  (toxins?)  flowing  in  the  general  circulation 
and  affecting  the  cardio-inhibitory  center  and  not  the  myocardium. 

Regarding  extrasystoles  in  pneumonia,  it  should  at  the  outset  be 
stated  that  this  disease  can  insidiously  cause  severe  cardiosclerosis 
(Chapter  XI) ;  but  this  does  not  apply  to  the  question  of  premature 
contractions  occurring  in  the  acute  stage  of  pneumonia.     Unless  cir- 


THE   ARRHYTHMIAS  99 

dilatory  symptoms  are  already  present,  pneumonic  patients  with  criti- 
cal or  post-critical  extrasystoles  do  not  suffer  from  cardiac  failure  as 
a  result  of  the  arrhythmia.  The  latter  usually  disappears  within  a  few 
days  without  any  treatment.  If  myocarditis  or  other  severe  pathologi- 
cal damage  in  the  heart  caused  these  extrasystoles,  symptoms  of  cir- 
culatory failure,  instead  of  being  absent,  would  be  prominent.  The 
present  theory  regarding  crises  is  that  the  system  is  at  such  times  sud- 
denly flooded  with  toxins  elaborated  in  the  pneumonic  area.  That 
the  cerebral  centers  become  involved  is  shown  by  critical  sweats  and 
vasomotor  symptoms.  Correlating  these  observations,  it  seems  most 
likely  that  the  extrasystoles  are  the  result  of  pneumonic  toxins  acting 
on  the  cardio-inhibitory  center. 

Among  drugs,  the  digitalis  bodies,  less  frequently  the  salicylates, 
produce  extrasystoles.  When  the  former  are  given,  the  arrhythmia 
is  usually  coincident  with  their  full  therapeutic  effect  (Chapter  XVI). 
Fright  and  epileptic  seizures,  overindulgence  in  coffee,  tea,  and  tobacco, 
are  additional  causes  of  premature  contractions.  The  latter  also  occur 
in  conjunction  with  the  vasomotor  symptoms  of  the  climacterium. 

There  still  remains  a  group  of  patients  in  whom  no  cause  for  extra- 
systoles can  be  discovered.  It  is  interesting  in  this  connection  to  note 
that  functional  extrasystoles,  even  though  they  later  disappear,  are 
apt  to  recur  after  any  slight  disturbance  (for  example,  overexertion, 
acute  indigestion)  which  reflexly  affects  the  normal  inhibitory  control. 

Therapy.  —  Such  underlying  diseases  as  gastric  disturbances,  ap- 
pendicitis, etc.,  naturally  require  their  appropriate  remedies ;  the 
presence  of  extrasystoles  in  no  wise  affects  the  usual  therapeutic  in- 
dications and  procedures.  Unless  extrasystoles  of  reflex  or  neurogenic 
origin  cause  such  subjective  sensations  as  "  fluttering  in  the  chest," 
transient  faintness,  etc.,  or  are  in  themselves  causes  of  circulatory 
failure  (an  exceedingly  rare  occurrence),  they  require  no  therapy.  When 
medication  is  indicated,  the  bromides  are  of  most  value.  Digitalis  has 
occasionally  been  advised  because  of  its  effect  in  increasing  vagus  in- 
hibition. 

Tetje  Bradycaedia 

The  term  has  already  been  defined  (Chapter  VII) .  It  may  appear  as 
a  rare  congenital  anomaly  in  patients  with  normal  hearts  and  circulation. 
A  sequential  rhythm  and  pulse  rate  between  45  and  60  per  minute  are 
sometimes  encountered  in  senile  cardiosclerosis.  Most  cases  of  true 
bradycardia  are  of  extracardiac  origin.  Patients  with  lead  colic  and 
gastro-intestinal  disorders,  accompanied  by  abdominal  pain,  belching,  or 
diarrhea,  are  apt  to  have  a  slow  pulse.  This  is  probably  due  to  reflex 
vagus  inhibition  from  excitation  of  gastric  and  intestinal  nerves. 

Catarrhal  jaundice  is  not  infrequently  accompanied  by  true  brady- 
cardia, and  is  usually  ascribed  to  toxic  myocarditis.  In  the  patients 
whom  I  have  observed,  there  was  no  evidence  of  the  latter  disease. 


100 


CLINICAL  CARDIOLOGY 


The  bradycardia  in  these  cases  may  be  ascribed  to  two  causes :  in  those 
with  cholemic  symptoms  it  is  probably  of  central  inhibitory  origin ;  in 
non-toxic  cases  with  painful  local  symptoms,  it  is  due,  I  believe,  to 
reflex  vagus  inhibition  from  excitation  of  the  nerve  filaments  surround- 
ing the  gall  bladder. 

Appendicitis.  —  Slight  bradycardia  with  pulse  rates  between  60  and 
65  per  minute  is  occasionally  encountered  in  appendicitis.  Myocardial 
involvement  or  quiescence  of  the  inflammatory  lesion  has  usually  been 
assumed  as  the  cause.  Unless  general  peritonitis  and  severe  toxemia 
are  present,  the  first  factor  seems  improbable.  Regarding  the  second 
factor  it  appears  more  likely  that  a  slow  pulse  is  an  indication  of  con- 
tinued and  active  excitation  at  the  inflammatory  focus  rather  than  an 
evidence  of  its  quiescence. 

Among  drugs,  the  digitalis  bodies  and  salicylates  cause  this  ar- 
rythmia  by  increasing  vagal  inhibition. 

Epileptics  occasionally  have  an  abnormally  slow  pulse.  This  is 
also  true  of  those  types  with  so-called  vago-vasal  attacks  (Gowers)  in 
which  there  are  no  convulsions,  but  vasomotor  symptoms,  vomiting, 
syncope,  and  pains  along  the  distribution  of  the  intercostal  nerves. 

A  slow  pulse  is  also  fairly  common  at  the  crises  of  febrile  pulmonary 
affections,  or  during  the  course  of  the  disease.  When  present  at  the 
crises,  I  believe  it  is  due  to  the  neurotropic  effect  of  the  toxins  liberated 
during  critical  defervescence. 

Therapy  for  bradycardia  is  only  indicated  when  the  slow  pulse  rate 
is  accompanied  by  subjective  symptoms.  Atropine  is  then  of  most 
value,  given  first  in  small,  later  in  increasing  doses,  until  the  full  physio- 
logical effect  has  been  reached. 


CLINICAL  AND  EXPERIMENTAL  CAUSES  OP  AURICULO- 
VENTRICULAR  HEART  BLOCK 

(a)  Destruction  of  the  A-  V  bundle  or  auric- 
ulo-nodal  junction  by  tumors  (benign 
or  malignant),  calcareous  deposits, 
fatty  and  inflammatory  infiltration, 
fatty  degeneration,  coronary  infarct, 
hemorrhage  in  the  node,  fibrosis. 

(b)  Severe  myocardial  degeneration.  —  De- 
struction of  the  branches  or  terminal 
arborizations  of  the  conduction  sys- 
tem. 

—  Morphine  —  Nicotine(  ?)). 


I.    Cardiac  Causes 


Extra- 
Cardiac 
Factors 


II. 
III. 


Drugs  (Digitalis 
(a)  Asphyxia. 

Chemical      f  Producing  acidosis. 
Poisons 


(b) 


IV. 

V. 

VI. 

I  VII. 


1.  toxins. 

[  anaphylotoxins. 
Interference  with  cerebral  circulation. 
Abnormal  pressure  on  the  cardio-inhibitory  center. 
Abnormal  pressure  on  the  vagus. 
Increased  vagal  inhibition. 

(a)  Digital  pressure  on  the  vagus. 

(b)  Peripheral  excitation. 


THE   ARRHYTHMIAS  101 

Heart  block  is  here  used  to  denote  auriculo-ventricular  dissociation, 
complete  or  incomplete;  it  does  not  refer  to  lengthened  conduction 
time,  blocked  auricular  beats,  or  to  sino-auricular  block.  I  have  made 
and  adopted  the  etiological  classification  given  above,  which  probably 
includes  the  great  majority  of  known  factors. 

I.  (a)  Any  lesion  which  completely  severs  or  destroys  the  main 
branch  of  the  conduction  system  produces  complete  heart  block.  If 
the  destruction  is  incomplete,  there  may  be  enough  healthy  strands  to 
carry  impulses  from  auricle  to  ventricle.  A  suddenly  deficient  cor- 
onary supply,  the  result  of  thrombosis,  infarct,  or  disease  of  the  nutrient 
artery  of  the  bundle  of  His,  can  so  profoundly  disturb  the  nutrition  of 
the  conduction  system  as  to  produce  transient  or  permanent  heart  block. 

I.  (6)  Just  as  fibrotic  and  calcareous  degeneration  in  the  conduction 
system  are  almost  invariably  accompanied  by  gross  pathological  changes 
in  the  ventricular  musculature,  so  in  extensive  cardiosclerosis  there 
are  often  fibrotic  and  other  degenerative  changes  in  the  connecting 
bundle.  Even  if  the  bundle  is  sufficiently  normal  to  convey  auricular 
impulses,  cardiosclerosis  in  itself  can  probably  produce  heart  block 
by  the  destruction  of  the  branches  or  terminal  arborizations  of  the 
conduction  system  in  the  ventricular  musculature,  in  this  manner  pre- 
venting impulses  from  reaching  their  final  destination.  On  the  other 
hand,  even  if  these  branches  and  their  ramifications  are  sufficiently 
normal  to  carry  impulses  from  auricle  to  ventricle,  the  ventricular 
musculature  may  be  so  diseased  as  not  to  be  capable  of  a  normal 
response.  Any  or  all  of  these  causes  (group  I  (&))  may  operate  in  those 
cases  of  heart  block  in  which  the  main  conduction  system  is  found  quite 
or  fairly  normal  upon  pathological  examination. 

Therapy.  —  When  syphilis  is  the  etiologic  factor,  vigorous  antiluetic 
treatment  —  salvarsan,  bichloride  injections,  and  iodide  of  potash  are 
indicated  (Chapter  XIV).  The  advisability  of  using  digitalis  and  atro- 
pine in  cardiac  disease  with  heart  block  is  discussed  in  a  subsequent 
chapter  (Chapter  XVI). 

II.  Digitalis  can  produce  complete  or  incomplete  block.  The 
arrhythmia  has  been  observed  not  only  in  those  patients  with  heart 
disease,  but  it  has  also  been  experimentally  induced  in  those  with  healthy 
hearts.  Complete  heart  block  has  been  induced  by  the  injection  of 
morphine  in  dogs,  and  was  there  regarded  as  an  effect  upon  the  cardio- 
inhibitory  center.  Morphine  poisoning  in  man  is  sometimes  accom- 
panied by  very  slow  pulse  rates.  These  have  never  been  graphically 
recorded ;  they  may  be  due  to  the  same  cause  found  in  the  animal  ex- 
periments; namely,  heart  block.  Tobacco  poisoning  is  occasionally 
accompanied  by  a  very  slow  pulse.  To  determine  its  precise  nature, 
graphic  tracings  are  necessary.  In  this  manner  it  may  in  the  future 
be  demonstrated  that  some  of  these  tobacco  arrhythmias  are  likewise 
due  to  heart  block. 

III.  (a)  In  animals,  the  experimental  production  of  asphyxia  is 


102  CLINICAL  CARDIOLOGY 

accompanied  by  varying  degrees  of  heart  block;  the  essential  cause 
is  assumed  to  be  nutritional  disturbances  from  lack  of  oxygen  in  the 
junctional  tissues.  With  our  present  imperfect  knowledge  of  the 
chemistry  of  the  blood,  it  is  impossible  to  state  whether  other  chemical 
factors  (group  III  (&))  can  act  similarly  in  the  production  of  heart  block 
by  profoundly  interfering  with  cardiac  nutrition.  Such  factors  are : 
abnormal  constituents  in  the  blood,  causing  lessened  blood  alkalinity 
(acidosis) ;  chemical  poisons  elaborated  in  infectious  diseases  (toxins) ; 
and  anaphylotoxins.  Regarding  acidosis,  I  have  several  times  observed 
heart  block  in  the  agonal  stages  of  patients  suffering  from  cardioscle- 
rosis and  nephritis,  in  whom  electrocardiograms  showed  very  rapid  and 
irregular  auricular  and  ventricular  activity  (Agonal  Arrhythmias,  Chapter 
VII).  Cyanosis  was  not  a  constant  factor.  Blood  examinations  for 
non-protein  nitrogen  and  other  products  were  not  made,  but  from  the 
clinical  syndrome,  it  seemed  that  retained  chemical  poisons  were  the 
essential  cause  of  the  arrhythmia.  With  reference  to  toxins,  it  has  been 
shown  experimentally  that  transfused  pneumonic  blood  profoundly 
impairs  cardiac  contractility.  I  have  had  occasion  to  study  two  cases 
which  have  a  bearing  upon  these  experimental  observations.  Both 
developed  heart  block  during  the  course  of  pneumonia.  In  one  an 
autopsy  was  performed.  Upon  macroscopic  examination  the  heart 
was  found  normal.  Careful  microscopical  examination  of  the  con- 
duction system  also  showed  that  it  was  normal.  Such  clinical  and 
experimental  observations  indicate  that  in  pneumonia,  at  any  rate, 
toxins  have  not  only  an  action  upon  the  cerebral  centers,  but  also  a 
local  action  upon  the  heart.  Block  may  then  result  from  interference 
with  nutrition  of  the  A-V  conduction  system  either  alone  or  in  con- 
junction with  the  remainder  of  the  cardiac  musculature.  Complete 
heart  block  has  been  produced  in  animals  by  producing  anaphylaxis; 
the  cause  is  assumed  to  be  due  to  an  effect  upon  the  heart  itself. 

IV.  Interference  with  Cerebral  Circulation.  —  This  factor  prob- 
ably operates  by  interference  with  nutrition  of  the  cardio-inhibitory 
center.  Sclerotic  changes  in  the  arteries  at  the  base  of  the  brain  is 
the  pathological  condition  most  frequently  observed.  In  one  reported 
case  of  heart  block,  few  changes  were  found  in  the  conduction  system 
or  cardiac  musculature,  the  cerebral  arteries  constituting  the  circle  of 
Willis  were  markedly  diseased,  the  brain  was  normal.  Tumors  and 
other  pathological  conditions  which  impede  cerebral  circulation  may 
have  a  similar  effect  in  producing  heart  block. 

V.  Abnormal  Pressure  on  the  Cardio-inhibitory  Center.  —  Such 
pressure  is  directly  or  indirectly  brought  about  by  cerebral,  cerebellar 
or  pontine  tumors,  ventricular  cysts,  meningitis,  hydrocephalus,  etc. 

VI.  Abnormal  Pressure  on  the  Vagus.  —  Tumors  and  adhesions 
are  the  most  likely  pathological  entities  which  may  have  this  effect. 
One  case  of  heart  block  from  pressure  on  the  vagus  has  been  reported ; 
a  large  tumor  in  the  anterior  mediastinum  involving  the  nerve  was  found. 


THE   ARRHYTHMIAS  103 

VII.  Increased  Vagal  Inhibition.  —  It  has  been  shown  that  in  chil- 
dren with  heart  disease,  digital  pressure  on  the  vagus  in  the  carotid 
sheath  may  be  followed  by  temporary  heart  block.  This  manoeuver 
probably  acts  by  causing  increased  vagal  inhibition.  A  case  has  also 
been  reported  in  which  swallowing  induced  heart  block  in  a  patient 
with  delayed  conduction  time.  These  are  examples  of  the  induction 
of  this  arrhythmia  resulting  from  direct  excitation  of  the  vagus  in  sus- 
ceptible individuals. 

(b)  Reflex  Peripheral  Excitation  of  the  Vagus.  —  I  have  observed 
cardiac  inhibition  with  the  production  of  block,  apparently  reflexly 
invoked  by  peripheral  stimulation  of  the  pneumogastric  branches  sup- 
plying the  stomach.  The  clinical  history  of  the  patient  showed  that 
the  pulse  had  been  normal  before  the  onset  of  tuberculous  peritonitis 
from  which  the  patient  suffered  when  he  first  came  under  observation. 
For  several  weeks  high  temperature  and  abdominal  pain  had  been 
present.  The  abdomen  was  opened,  and  fluid  evacuated.  Some  weeks 
after  operation,  the  symptoms  of  tuberculous  peritonitis  entirely  sub- 
sided. Two  years  later  the  patient  was  killed  in  an  accident.  Com- 
plete heart  block,  as  shown  by  polygraphic  and  electrocardiographic 
curves,  was  present  before  and  after  the  operation,  and  up  to  the  time 
of  the  patient's  death.  The  presence  of  the  arrhythmia  caused  no  symp- 
toms. A  necropsy  was  performed ;  the  lungs  were  found  normal ;  a 
mass  of  enlarged  non-suppurating  tuberculous  glands  adherent  to 
stomach  and  intestines  was  found.  Careful  macroscopic  examination 
showed  the  heart  to  be  absolutely  normal.  At  the  present  time  the 
microscopical  examination  has  not  been  completed  ;  but  careful  scrutiny 
of  the  conduction  system  showed  the  absence  of  any  gross  lesion. 
Toxemia  as  a  cause  of  the  heart  block  could  be  excluded,  for  the  patient 
was  clinically  well,  had  had  no  temperature,  and  was  at  work  for  months 
prior  to  his  death.  Weighing  the  pathological  and  clinical  data,  it 
seems  probable  to  me  that  the  heart  block  was  due  to  abnormally  in- 
creased vagal  inhibition  reflexly  excited  by  involvement  of  peripheral 
nerve  filaments  in  the  tuberculous  foci. 

Therapeutically  atropine  sulphate  should  be  tried  in  all  cases  of 
heart  block ;  it  should  be  given  hypodermically  until  the  full  physio- 
logical effect  is  reached.  Appropriate  treatment  should  be  directed 
against  the  individual  etiological  factors. 

Prolonged  Conduction  Time 

Among  drugs,  digitalis  occasionally  produces  this  arrhythmia.  The 
chief  cardiac  cause  is  myocardial  degeneration ;  indeed,  a  prolonged 
a-c  interval  may  be  the  only  evidence  of  this  disease.  Prolonged  con- 
duction time  is  encountered  during  the  course  of,  or  immediately  after, 
attacks  of  rheumatic  endocarditis.     It  is  also  met  with  in  acute  or  sub- 


104  CLINICAL  CARDIOLOGY 

acute  nephritis  in  which  there  are  none  of  the  usual  clinical  manifesta- 
tions of  myocarditis.  The  arrhythmia  is  occasionally  of  neurogenic 
origin.  Therapy  is  indicated  for  the  symptoms  of  myocarditis  or  for 
other  etiological  factors,  but  not  for  the  prolonged  conduction  time. 

Shortened  Conduction  Time 

I  have  found  this  arrhythmia  especially  frequent  in  exophthalmic 
goiter  (Chapter  IV).  The  fact  that  experimental  excitation  of  the 
right  accelerator  nerve  is  accompanied  by  a  slightly,  and  of  the  left, 
by  a  considerably,  shortened  conduction  time  is  doubtless  of  etio- 
logical significance  in  exophthalmic  goiter,  in  which  the  chief  symp- 
toms are  due  to  excitation  of  the  sympathetic  system.  With 
shortened  conduction  time  tachycardia  is  usually  present ;  the  latter 
with  other  clinical  manifestations  may  require  medication,  the  short- 
ened conduction  time  in  itself  does  not. 


Auricular  Fibrillation 

This  is  the  usual  arrhythmia  accompanying  decompensation  in 
rheumatic  mitral  stenosis  in  the  young  and  middle-aged.  It  is  some- 
times found  in  children;  I  have  seen  several  instances  in  patients 
between  10  and  12  years  of  age.  The  frequent  association  of  auricular 
fibrillation  with  mitral  stenosis  has  never  been  satisfactorily  explained. 
It  is  known  that  stenosis  is  often  accompanied  by  hypertrophy  and 
dilatation  of  one  or  both  auricles.  Destructive  changes  in  the  sino- 
auricular  node,  similar  to  those  observed  in  older  patients  with  cardio- 
sclerosis and  auricular  fibrillation,  have  been  described  in  isolated  in- 
stances. In  addition  to  these  profound  pathological  changes,  it  appears 
to  me  that  mechanical  auricular  overdistention  (to  which  attention 
has  not  been  directed)  may  play  an  etiological  role  in  the  production 
of  the  arrhythmia.  Overdistention  may,  for  example,  prevent  the 
proper  performance  of  coordinate  rhythmical  contractions  to  normal 
stimuli,  and  in  their  stead,  the  answer  to  stimulus  production  consists 
in  the  irregular,  vermicular,  incoordinate  contractions  characteristic 
of  auricular  fibrillation.  The  auricular  structure  and  the  method  of 
transmission  of  the  excitation  wave  (Chapter  VI)  explain  fibrillation 
in  both  auricles  after  one  has  been  affected. 

Auricular  fibrillation  is  found  less  frequently  in  rheumatic  aortal 
lesions.  It  is  an  extremely  common  arrhythmia  in  all  types  of  cardio- 
vascular disease  in  the  aged  (Chapter  XV). 

In  cardiac  disease  with  decompensation  auricular  fibrillation  is 
usually  permanent.  It  may,  however,  be  transient  or  occur  only  in 
attacks.  I  have  observed  such  attacks  lasting  several  days  in  two  cases  of 
aortic  aneurism.   In  one,  it  occurred  with  the  gradual  onset  of  severe  de- 


THE  ARRHYTHMIAS  105 

compensation ;  in  the  other  /there  was  no  discoverable  cause  for  the  attacks. 
Another  instance  of  transient  auricular  fibrillation  was  that  of  a  woman 
of  60,  a  sufferer  from  mild  myocardial  insufficiency,  who  had  been  oper- 
ated upon  for  empyema  of  the  gall-bladder.  Following  the  operation, 
there  were  several  distinct  attacks  of  broncho-pneumonia,  the  onset 
of  each  being  marked  by  a  moderate  rise  of  temperature,  and  by  auric- 
ular fibrillation  lasting  one  day.  In  mitral  stenosis,  pari  passu 
with  fresh  exacerbations  of  endocarditis,  auricular  fibrillation  may 
occur.  Thus,  in  a  man  of  45  with  a  double  mitral  lesion,  from  whose 
blood  a  non-hsemolytic  streptococcus  was  isolated,  each  sharp  febrile 
invasion  was  accompanied  by  an  attack  of  auricular  fibrillation ;  these 
attacks  lasted  several  hours  or  days.  Patients  with  mitral  disease 
who  suffer  from  acute  febrile  disturbances  of  non-rheumatic  origin  are 
also  prone  to  attacks  of  this  arrhythmia ;  these  may  last  throughout  the 
fever.  I  have  seen  two  such  instances:  one,  a  patient  with  mitral 
regurgitation,  the  other  with  mitral  stenosis;  both  developed  fibril- 
lation during  erysipelas.  Auricular  fibrillation  may  also  be  an  initial 
symptom  of  coronary  embolism  or  thrombosis. 

From  these  observations  it  is  evident  that  in  diseased  hearts  any 
additional  insult  to  the  endocardium,  myocardium,  or  coronary  arteries 
may  be  accompanied  by  auricular  fibrillation.  The  permanence  of  the 
arrhythmia  may  depend  upon  the  severity  or  permanence  of  the  path- 
ological damage. 

The  sovereign  remedy  for  this  irregularity  when  found  in  decom- 
pensated cardiac  disease  is  digitalis.  The  details  of  its  administration 
are  elsewhere  described  (Chapter  XVI).  I  have  occasionally  added 
large  doses  of  bromide,  or  have  initiated  digitalis  medication  with  one 
or  two  large  doses  of  morphine  when  patients  were  very  dyspnoeic  or 
restless. 

Articular  fibrillation  occurs  very  exceptionally  in  patients  with 
normal  hearts.  I  have  observed  several  cases  of  temporary  auricular 
fibrillation  coming  on  at  the  critical  defervescence  of  lobar  pneumonia ; 
there  was  no  evidence  of  heart  disease  or  heart  failure  during  the  entire 
course  of  the  disease  or  during  convalescence.  Some  of  these  patients 
were  examined  months  after  the  pneumonia.  Their  hearts  were  found 
perfectly  normal.  Temporary  or  permanent  auricular  fibrillation  is  also 
fairly  common  in  exophthalmic  goiter.  Apparently  here  influences 
affecting  neurogenic  cardiac  control  are  the  essential  factors.  I  have 
likewise  seen  auricular  fibrillation  in  a  man  with  a  normal  heart  who 
was  a  very  heavy  smoker.  A  case  due  to  hydrogen  sulphide  poison- 
ing in  a  man  with  a  normal  heart  has  recently  been  reported. 

In  those  cases  of  fibrillation  which  are  apparently  of  toxic  or  of 
neurogenic  origin,  I  have  found  very  little  value  in  digitalis ;  the  pulse 
or  ventricular  rate  was  not  appreciably  affected ;  dyspnoea,  if  present, 
continued.  Large  doses  of  bromide,  alone  or  combined  with  small 
doses  of  codeine,  seemed  occasionally  of  value. 


106  CLINICAL  CARDIOLOGY 


Simple  Tachycardia  —  Ordinary  Pulse  Acceleration 

Rapid,  regular  pulse  rates  usually  range  between  120  and  180  per 
minute,  and  are  the  result  of  excitation  of  the  accelerator  nerves.  The 
causes  are  manifold.  Excitement,  fright,  overexertion,  fever  are  some 
of  the  commoner.  In  exophthalmic  goiter,  tachycardia  is  one  of 
the  cardinal  symptoms.  Gastro-intestinal  disturbances  of  functional 
or  organic  nature  are  frequently  accompanied  by  rapid  heart  action. 
Persistent  tachycardia  may  be  the  only  clinical  evidence  of  a  fresh  ex- 
acerbation of  an  old  endocarditis.  Cardiac  decompensation  from  any 
source  is  often  accompanied  by  moderate  tachycardia,  and  is  sometimes 
the  forerunner  of  other  arrhythmias.  Among  other  causes  of  rapid  heart 
action  are  dyspnoea  from  pulmonary  disease,  tabagism,  overindulgence 
in  tea  and  coffee,  and  atropine. 

Pulse  acceleration  requires  medication  only  when  the  pulse  rate  is 
high  or  subjective  sensations  are  present.  When  tachycardia  is  due  to 
fever,  digitalis  has  no  effect  in  reducing  the  pulse  rate.  The  bromides 
or  codeine  are  occasionally  efficacious  in  slowing  the  heart  in  such  cases. 
Digitalis  may  decrease  the  pulse  rate  when  the  tachycardia  is  due 
to  cardiac  decompensation. 


Paroxysmal  Tachycardia 

This  is  more  often  of  functional  than  of  organic  origin.  Its  most 
frequent  extracardiac  cause  is  acute  indigestion,  and  is  then  apparently 
due  to  reflex  excitation  of  the  accelerators.  I  have  seen  several  patients 
in  whom  every  attack  of  indigestion  was  accompanied  by  this  arrhythmia. 
In  a  woman  of  50  with  abdominal  cancer,  gastric  symptoms  and  severe 
secondary  ansemia,  slight  fright  or  nervous  excitement  would  frequently 
initiate  an  attack.  At  necropsy,  the  cardiac  musculature  was  somewhat 
pale,  otherwise  the  heart  was  normal.  In  another  patient,  a  woman 
of  45  with  a  luetic  history  and  positive  blood  Wassermann,  sudden  gas- 
tric attacks  also  initiated  paroxysmal  tachycardia.  It  is  interesting  to 
note  that  during  these  attacks  there  was  marked  dilatation  of  the  left 
pupil,  an  evidence  of  sympathetic  nerve  excitation. 

In  addition  to  treatment  directed  to  the  cause  (gastric  sedatives, 
etc.),  sudden  firm* pressure  over  the  vagus  in  its  course  in  the  neck  may 
occasionally  suddenly  arrest  the  arrhythmia.  Pressure  on  the  right  side 
should  be  first  tried ;  if  this  does  not  succeed,  pressure  should  be  exerted 
over  the  left  vagus.  Similarly,  pressure  on  the  right  or  left  eyeball 
can  be  tried  in  the  attempt  to  induce  the  oculo-cardiac  reflex.  Inducing 
emesis  may  also  affect  the  vagus  control.  Strophanthin  may  be  em- 
ployed hypodermically  or  intravenously  because  of  its  quick,  powerful 
effect  in  increasing  vagus  inhibition.  If  these  procedures  or  drugs  are 
unsuccessful,  morphine  or  the  bromides  are  indicated. 


THE  ARRHYTHMIAS  107 

Auricular  Flutter 

This  arrhythmia  is  most  frequent  in  older  people  with  cardiosclerosis 
in  the  period  of  decompensation.  It  can  also  occur  during  the  course 
of  acute  endocarditis  without  decompensation.  Occasionally  auricular 
flutter  is  of  functional  origin.  In  acute  endocarditis,  digitalis  does  not 
control  the  arrhythmia.  Since  the  drug  has  not  been  employed  in  flutter 
of  functional  nature,  nothing  is  known  of  its  effect  in  such  cases.  In 
auricular  flutter  with  decompensation  and  cardiosclerosis,  digitalis 
(Chapter  XVI)  is  of  very  great  value.  Its  administration  is  then  fol- 
lowed by  auricular  fibrillation ;  if  the  drug  is  then  discontinued,  normal 
rhythm  is  resumed,  and,  coincidently,  return  to  compensation. 

Ventricular  Escape  —  Independent  Ventricular  Activity 

A  brief  report  of  a  case  of  this  interesting  and  rare  arrhythmia 
follows.  The  etiological  factors  involved  in  this  and  other  patients 
with  this  arrhythmia  is  discussed  in  the  comment  following  the  case 
report. 

S.  P.,  male,  aged  20,  was  first  observed  on  February  4, 1913.  He  had 
measles  when  3  years  old  and  typhoid  when  10 ;  otherwise  there  was  no 
history  of  any  previous  illness.  He  was  not  addicted  to  tea,  coffee, 
tobacco,  or  alcohol.  Five  days  previously  he  developed  a  typical  attack 
of  acute  articular  rheumatism  involving  the  ankles,  wrists,  knees,  and 
elbows.  The  attack  was  accompanied  by  fever ;  there  were  no  chills 
or  gastric  disturbances. 

Except  for  swelling  and  redness  of  the  inflamed  joints,  the  general 
and  neurological  examination  revealed  nothing  abnormal.  There  was 
no  urethral  discharge.  The  complement-fixation  test  for  gonorrhoea 
was  negative.  The  cardiac  outline  was  normal  to  percussion,  the  apex 
beat  was  in  the  fifth  interspace,  8.5  cm.  from  the  midsternal  line ;  the 
heart  sounds  were  normal ;  the  pulse  was  rhythmical.  The  systolic 
and  diastolic  blood  pressures  were  within  normal  limits.  The  tempera- 
ture ranged  between  101°  and  103°.  There  was  no  dyspnoea.  The 
patient  did  not  appear  very  ill.  Sodium  salicylate  in  moderate  doses 
was  given  for  two  days. 

Two  days  after  hospital  admission,  a  transient  pulse  irregularity 
appeared.  Six  days  thereafter,  it  reoccurred  and  clinically  resembled 
extrasystoles ;  no  tracings  were  made  at  that  time.  February  12,  the 
irregularity  occurred  every  third  or  fourth  beat.  From  that  day  fre- 
quent poly  graphic  and,  later,  electrocardiographic  tracings  were  taken. 
February  14,  for  the  first  time  a  rough  blowing  systolic  murmur  was 
heard  at  the  apex.  Occasionally  there  were  runs  of  from  three  to  twelve 
stronger  thumping  beats  unaccompanied  by  the  murmur;  studies  of 
the  tracings  showed  that  these  beats  were  due  to  simultaneous  action 
of  auricle  and  ventricle.     Four  days  later  the  arrhythmia  appeared  only 


108  CLINICAL   CARDIOLOGY 

infrequently  and  the  systolic  murmur  had  almost  entirely  disappeared. 
The  patient  left  the  hospital  feeling  well. 

As  possible  causes  for  the  production  of  automatic  ventricular  action, 
neurogenic,  toxic,  and  organic  factors  require  consideration.  A  neu- 
rogenic factor  in  the  sense  of  a  so-called  neurosis  due  to  extracardial 
conditions  (for  example,  gastric  disorders)  causing  abnormal  excitation 
in  the  centripetal  arm  of  a  reflex  arc,  can  be  here  dismissed  because  of 
the  type  of  the  disease,  its  course,  and  the  definite  completion  of  the 
arrhythmia  with  the  end  of  the  rheumatic  attack.  Concerning  toxins 
their  action  seems  to  depend  upon  their  complicated  chemical  composi- 
tion and  upon  intricate  chemical  reactions  taking  place  in  the  body.  By 
analogy,  it  seems  possible  that  a  rheumatic  toxin  may  also  produce  a 
similar  arrhythmia,  though  there  is  no  evidence  for  the  assumption  in 
this  case.  Concerning  an  organic  cause  for  the  arrhythmia,  it  is  recalled 
that  the  patient  developed  a  loud  systolic  murmur  at  the  apex,  one  week 
after  the  appearance  of  the  arrhythmia  ;  the  murmur  remained  for  two 
days,  then  gradually  disappeared.  It  also  disappeared  when  auricle 
and  ventricle  contracted  simultaneously,  an  apparent  corroboration 
that  it  was  due  to  mitral  insufficiency,  organic  or  relative  in  nature. 
It  is  not  my  intention  to  discuss  cardiac  murmurs  at  any  length  in  this 
connection.  Briefly,  systolic  apical  murmurs  which  occur  during  the 
course  of  any  febrile  disease,  and  then  disappear  without  evidence  of 
an  organic  cardiac  lesion,  are  by  no  means  infrequent.  On  the  other 
hand,  organic  murmurs  usually  increase  in  intensity  and  do  not  dis- 
appear. The  occurrence  of  the  murmur  in  conjunction  with  acute 
articular  rheumatism  makes  its  presence  suspicious  of  some  transient 
valvular  or  myocardial  involvement.  Rheumatic  infections  cause 
myocardial  inflammation  in  the  form  of  submiliary  myocardial  nodules 
(Aschoff  bodies,  Chapter  XII).  Healed  or  healing  isolated  Aschoff 
bodies  have  been  found  on  the  interventricular  septum  in  hearts 
which  were  the  subjects  of  rheumatic  reinfection.  During  their  in- 
flammatory state,  if  situated  close  to  or  even  partly  involving  the 
bundle  of  His  before  its  division,  they  can  conceivably  cause  local 
irritation  sufficient  to  produce  occasional  ventricular  automatism  with 
beats  of  supraventricular  origin.  The  bundle,  however,  need  not  be 
sufficiently  compromised  to  prevent  the  idioventricular  impulse  from 
following  its  normal  course  in  the  conduction  system  —  a  fact  which 
probably  accounts  for  identical  electrocardiographic  complexes  of  all 
beats,  rhythmic  and  arrhythmic. 

Right  and  left  vagus  pressure  had  no  effect  on  auriculo-ventricular 
sequence.  One  of  the  atropine  experiments  was  followed  by  a  number 
of  independent  ventricular  contractions,  with  no  marked  difference 
between  ventricular  and  auricular  rates.  This  observation  does  not 
necessarily  exclude  the  possibility  of  an  organic  cause  for  ventricular 
automatism,  because  an  irritative  lesion  which  does  not  entirely  and 
permanently  compromise  the  bundle  may  upset  normal  nerve  control 


THE   ARRHYTHMIAS  109 

and  mechanism  and  make  the  latter  susceptible  to  atropine  poisoning. 
It  would  thus  seem  that  the  automatic  ventricular  mechanism  was  not 
sufficiently  sensitive  to  respond  to  vagus  pressure,  but  that  atropine 
poisoning  prevented  the  inhibitory  vagus  control  and  permitted  ventric- 
ular escape. 

Summarized,  a  case  of  independent  ventricular  activity  is  described  ; 
the  lowest  ventricular  rate  is  56  per  minute,  the  usual  rate  is  60  and 
remains  so  whether  ventricular  automatism  is  present  or  not.  The 
electrocardiographic  complexes  of  all  beats  are  identical.  At  one  time 
atropine  administration  is  followed  by  ventricular  escape.  The  occur- 
rence of  automatic  activity  during  the  course  of  acute  articular  rheu- 
matism and  its  disappearance  later,  and  a  study  of  the  physical  signs 
make  it  probable  that  a  small  transient  myocardial  inflammatory  focus 
at  or  near  the  auriculo-ventricular  bundle  is  the  irritative  cause  of  the 
abnormal  mechanism. 

Therefore  it  may  be  stated  that  transient  independent  ventricular 
activity  may  occur  with  no  change  in  the  path  followed  by  the  idio- 
ventricular impulse,  with  no  difference  of  rate  between  normal  and  ab- 
normal beats,  and  with  no  marked  retardation  of  the  auricular  rate. 

REFERENCES 
Chapter  VIII 

Einthoven,  W. :     Thierische   Elektrizitaet ;     Verhandlungen    der    Gesellschaft 

Deutscher  Naturforscher  und  Aerzte,  1911,  80. 
Gowers,  W.  R. :   The  Borderland  of  Epilepsy. 
Lewis,  T. :   Lectures  on  the  Heart ;  21. 
Mackenzie,  J. :   Diseases  of  the  Heart. 
Mathison,  G.  C. :    The  Cause  of  the  Heart  Block  occurring  during  Asphyxia ; 

Heart,  1910-1911,11,54. 
Neuhof ,  S.  :  Functional  Heart  Block  in  Pneumonia ;  Journal  of  the  American 

Medical  Association,  1914,  LXIII,  577. 
Neuhof,   S. :    Clinical  Observations  of  Reflex  Vagus  Phenomena  grouped  in 

Symptom  Complexes ;    American  Journal  of  the  Medical  Sciences,  1912, 

CXLII,  724. 
Neuhof,  S. :  Gastric  Neuroses  ;  New  York  Medical  Journal,  1914,  C,  365. 
Neuhof,  S.  :    Etiology,  Diagnosis  and  Therapy  of  the  Commoner  Arrhythmias  ; 

The  Post-Graduate,  1913,  XXVIII,  1103. 
Neuhof,  S. :    Extrasystoles :    Clinical  Observations,  Etiology  and  Treatment ; 

New  York  Medical  Journal,  1913,  XCVII,  545. 
Oppenheimer,  B.  S.,  and  Williams,  H.  B. :    Prolonged  Complete  Heart  Block 

without  Lesion  of  the  Bundle  of   His  and  with  Frequent  Changes  in  the 

Idioventricular  Electrical  Complexes ;    Proceedings  Soeietv  Experimental 

Biology  and  Medicine,  1913,  X,  86. 
Robinson,  G.  C,  and  Draper,  G. :  The  Effect  of  Vagus  Stimulation  on  the  Hearts 

of  Children  with  Chronic    Valvular    Disease ;     Journal  of  Experimental 

Medicine,  1912,  XV,  12. 
Robinson,  G.  C. :    Transient  Auricular  Fibrillation ;    Journal  of  the  American 

Medical  Association,  1916,  LXVI,  1611. 
Rothberger,  C.  J.,  and  Winterberg,  H. :   Ueber  die  Beziehung  der  Herznerven 

zur  Form  des  Elektrokardiogramms  ;  Archiv  fur  die  gesammte  Physiologie, 

CXXXV,  506. 


CHAPTER  IX 
ORTHODIASCOPY  AND  FLUOROSCOPY 

Definition  of  Orthodiascopy.  —  Orthodiascopic  examination  con- 
sists essentially  in  a  method  of  outlining  a  viscus  by  means  of  parallel 
roentgenograph^  rays ;  in  this  manner  the  exact  size  of  the  organ  is 
reproduced.  With  the  tube  stationary  and  near  the  patient,  the  rays 
are  divergent;  hence  the  object  to  be  examined  becomes  artificially 
enlarged.  This  distortion  is  magnified  if  the  organ  itself  be  large,  for 
the  impinging  rays  become  still  more  divergent;  an  hypertrophied 
heart,  for  example,  produces  a  disproportionately  enlarged  shadow. 
This  was  well  exemplified  in  a  case  in  which  the  roentgenogram  taken 
two  days  before  death  showed  the  shadow  of  a  tremendously  enlarged 
heart.  At  necropsy  the  heart  was  found  only  moderately  enlarged; 
pericarditis  causing  a  tightly  adherent  pericardium  prevented  agonal 
cardiac  dilatation  which  might  have  been  assumed  as  the  cause  for  the 
enlarged  roentgenographic  shadow. 

Two  methods  of  avoiding  distorted  images  have  been  devised. 
(1)  Teleroentgenography :  the  X-ray  tube  is  placed  about  6  feet  from 
the  patient,  so  that  the  rays  reach  the  organ  approximately  parallel. 
This  method  has  given  satisfactory  and  fairly  accurate  results.  (2) 
Orthodiascopy :  the  focus  of  the  X-ray  tube  and  the  center  of  the  screen 
are  adjusted  so  as  to  be  in  a  straight  line ;  the  X-ray  tube  and  the 
fluoroscopic  screen  move  together.  Any  series  of  points  which  outline 
a  viscus  are  brought  in  alignment  so  that,  with  the  movement  of  the 
tube  and  screen,  parallel  and  not  divergent  rays  impinge  upon  the 
organ  and  reach  the  observer. 

Orthodiascopy 

The  Groedel  apparatus  is  the  one  I  have  found  most  suitable  for 
orthodiascopy  of  the  heart.  Examinations  can  be  made  in  the  sitting, 
standing,  or  lying  postures.  For  convenience,  and  the  comfort  of  the 
patient,  I  prefer  the  sitting  position.  After  the  patient  is  properly 
seated  (see  legend,  Fig.  202,  Plate  XVII),  the  room  darkened,  and  the 
electric  foot  switch  turned  on,  a  rapid  survey  is  first  taken  of  the  entire 

no 


PLATE   XVII 


Fig.  202.  —  Groedel  Orthodiascope,  front  view. 

The  patient  sits  with  his  feet  resting  comfortably  on  the  adjustable  step  (ST)  ;  the  side 
plates  (SP)  can  be  lowered  or  raised  and  pushed  in  or  out ;  they  are  placed  so  that  they 
fit  snugly  in  the  axilla?  and  against  the  chest  of  the  patient.  The  fluoroscopic  screen 
(FS)  is  grasped  by  the  finger  of  the  right  hand  in  a  small  ring  (R) .  The  bar  B'  carrying 
the  screen  is  connected  by  the  hollow  crossbar  (CB)  with  the  bar  B"  ;  the  latter  carries 
the  X-ray  tube  so  that  any  motion  imparted  to  the  fluoroscopic  screen  by  the  observer 
moves  the  X-ray  tube  as  well.  By  loosening  the  nut  (N)  the  bar  (B')  may  be  slid  along 
the  crossbar  and  the  screen  may  be  placed  any  convenient  distance  from  the  patient's 
chest. 

RB  =  rubber  bulb  used  for  marking  purposes ; 

SC  =  sliding  counterweights  so  that  the  screen  and  X-ray  bars  may  be  properly 
counterpoised ; 
C  =  cranks  used  to  place  the  table  in  the  horizontal  position  if  necessary ; 
LS  =  leveling  screws ; 
FSw  =  the  electrical  foot  switch. 


> 

X 

H 

Eh 


^ 


ORTHODIASCOPY  AND   FLUOROSCOPY  111 

heart  by  moving  the  fluoroscopic  screen  over  the  cardiac  area.  The 
cardiac  outline  is  then  systematically  mapped  out.  The  central  spot 
of  the  screen  (F.S.  Fig.  202,  Plate  XVII)  is  brought  over  the  edge  of  the 
area  to  be  delimited ;  this  point  is  then  marked  by  pressing  the  rubber 
bulb  with  the  left  hand.  My  practice  is  to  start  the  tracing  on  the  left 
side  by  dotting  out  the  upper  outer  limit  of  the  aorta,  then  continuing 
downwards  and  marking  the  other  curves  of  the  heart  until  the  entire 
left  side  is  outlined.  To  expose  the  lowest  part  of  the  apex,  the 
patient  is  asked  to  hold  his  breath  at  the  end  of  deep  inspiration.  The 
upper  right  border  of  the  aorta,  then  the  remainder  of  the  right  border 
of  the  heart,  are  mapped  out  down  to  the  diaphragm.  Finally,  the  line 
of  the  diaphragm  is  mapped  out  on  each  side.  The  cardiac  contour  is 
best  dotted  out  during  the  time  of  systolic  contraction.  There  is  no  dan- 
ger of  X-ray  burns  since  the  amount  of  current  used  is  small  (about  10 
amperes).  The  entire  orthodiascope  tracing  generally  requires  about  two 
minutes.  During  the  examination  and  for  a  minute  or  two  thereafter, 
the  observer  can  carefully  study  the  heart  action,  and  thus  not  only  gain 
important  data  regarding  the  various  types  of  contractility,  especially 
of  the  left  ventricle  and  aorta,  but  also  fluoroscopically  study  shadows, 
the  interpretation  of  which  may  be  uncertain  in  a  roentgenogram. 

The  details  of  the  marking  mechanism  are  shown  in  Fig.  203  (Plate 
XVIII). 

Orthodiascopic  Tracing  of  the  Normal  Heart.  —  The  contour  of 
the  normal  heart  and  aorta  is  an  irregular  oblique  ovoid ;  its  larger 
end  is  directed  downwards  and  to  the  left  (Fig.  204).  The  outline  is 
made  up  of  several  curves  formed  by  different  portions  of  the  heart. 
On  the  right  side  above,  we  find  the  ascending  aorta,  which  forms  a 
curve  with  a  slight  outward  convexity  (A  1,  Fig.  204).  Above  it,  the 
great  vessels  are  sometimes  seen  as  indefinite  shadows.  Very  rarely, 
the  superior  vena  cava  is  visible  as  an  attenuated  shadow  stretching 
across  the  aorta.  Below  the  ascending  aorta  is  the  curve  formed  by  the 
right  auricle  (JR. A,  Fig.  204).  It  is  usually  a  well-defined  arc  and  forms 
an  acute  angle  with  the  arch  of  the  diaphragm.  In  cases  of  extreme 
right  ventricular  enlargement,  or  in  pericarditis  with  effusion,  this 
angle  may  be  obliterated.  The  left-sided  silhouette  is  composed  of 
four  more  or  less  distinct  curves.  From  above  downwards,  these  are 
the  aortic  arch  {A  2,  Fig.  204),  the  pulmonary  artery  (P. A),  the  left 
auricular  appendix  and  auricle  (L.A),  and  the  left  ventricle  (L.V). 
The  arch  of  the  aorta  protrudes  slightly  beyond  the  left  sternal  border, 
describing  a  convex  arc ;  if  the  aorta  curves  sharply  downwards 
and  backwards  to  reach  the  spine,  this  arc  assumes  a  knoblike  promi- 
nence. The  pulsatile  excursions  are  slight  (about  .5  centimeter)  and 
require  careful  scrutiny  in  order  to  identify  them.  The  average  length 
of  the  arch,  visible  as  a  separate  shadow,  is  from  3  to  5  centimeters. 
The  left  margin  of  the  descending  aorta  can  sometimes  be  traced  down- 


112 


CLINICAL   CARDIOLOGY 


wards  for  several  centimeters  as  a  lighter  shadow;  in  exceptional  in- 
stances, it  is  dimly  seen  as  a  pulsating  shadow  behind  the  body  of  the 
left  ventricle.  Beneath  the  aortal  arch  and  distinguished  from  it  as 
a  much  smaller  and  less  convex  silhouette  is  the  pulmonary  artery; 
its  average  visible  length  is  from  2  to  3  centimeters.  The  contour  of 
the  pulmonary  artery  is  distinguished  from  that  of  the  underlying  left 

auricle  by  the  difference  in  pul- 
sation time.  The  left  auricular 
curve  is  obtusely  oblique  and  va- 
riable in  size;  it  consists  mainly 
of  the  left  auricular  appendix,  but 
sometimes  also  includes  part  of 
the  left  auricle.  The  left  ventric- 
ular curve  constitutes  the  greater 
portion  of  the  left  ventricle,  and 
forms  its  ovoid  end.  The  extent 
to  which  the  left  ventricle  is  visi- 
ble depends  upon  the  shape  of  the 
heart  and  the  mobility  of  the 
diaphragm.  In  stout  individuals 
with  thick  abdominal  walls,  dia- 
phragmatic excursion  is  usually 
limited,  and  the  apex  of  the  heart 
may  not  be  visible ;  in  thin  indi- 
viduals with  good  diaphragmatic 
mobility  the  entire  left  ventricu- 
lar surface  including  the  apex  is 
plainly  seen  at  the  end  of  inspira- 
tion. 

Orthodiascopic  Standards.  — 
In  order  accurately  to  determine 
the  standard  size  of  the  heart, 
numerous  statistical  studies  and 
measurements  of  orthodiascopic 
tracings  have  been  made.  For  this  purpose,  oblique  and  other  diameters 
of  the  cardiac  ovoid  (Fig.  204)  have  been  devised  and  measured  ;  from 
these,  attempts  have  been  made  to  establish  normal  cardiac  areas.  The 
diameter  representing  the  greatest  width  of  the  heart  (B  1  +  B  2,  Fig. 
204)  depends  for  its  accuracy  upon  the  left  auricular  curve ;  this  is  a 
variable  quantity  even  in  normal  individuals  and  hence  unreliable 
as  a  standard  for  measurement.  Some  observers  have,  therefore, 
chosen  the  largest  oblique  diameter  (L.O,  Fig.  204)  and  the  distance 
of  the  cardiac  borders  from  the  median  line  (M.R,  M.L)  as  being 
more  exact.  These  axes  have  been  studied  principally  by  Groedel, 
Dietlin,  and  Veith  in  individuals  of  both  sexes,  of  various  ages,  weights, 
and  size,  with  varying  types  of  thorax,  and  following  different  voca- 


Fig.  204.  —  Orthodiascopic    tracing 
normal  heart. 


the 


A\ 
R.A 
A2 
P.A 
L.A 
L.V 
M.R 

M.L 

L.O 

B  1+52 


=  ascending  aorta ; 

=  right  auricle ; 

=  aortal  arch ; 

=  pulmonary  artery ; 

=  left  auricular  appendix ; 

=  left  ventricle ; 

=  greatest  distance  fro.m  median 
line  to  the  right ; 

=  greatest  distance  from  median 
line  to  the  left ; 

=  longest  oblique  diameter  of  the 
cardiac  ovoid ; 

=  greatest  width  of  the  orthodia- 
scopic tracing. 


ORTHODIASCOPY  AND   FLUOROSCOPY 


113 


tions.     Groedel  has  found  the  following  figures  in  the  vertical  ortho- 
diagrams : 


In  the  adult  male 
Male  youths 
Female  adults 
Young  females    . 


M.R 


4.G  cm. 
4.1  cm. 
3.9  cm. 
3.7  cm. 


M.L 


8.4  cm. 
7.8  cm. 
8.0  cm. 
7.2  cm. 


L.o 


14  cm. 
12.7  cm. 
12.9  cm. 
12.1  cm. 


In  these  measurements,  a  certain  correlation  has  been  found  between 
the  cardiac  area,  and  size  and  weight  of  the  individual.  However, 
there  are  important  considerations  which  tend  to  lessen  the  value  of 
measurements  as  standards.  Size,  weight,  type  of  thorax,  and  occupa- 
tion are  factors  which  have  already  been  mentioned.  In  these  alone 
there  is  a  wide  range  of  maximal  and  minimal  measurements  which 


s&\ 


Fig.  205.  —  Orthodiascopic  tracing  of  long 
and  slender  heart. 


Fig.   206.  —  Copy   of    an    orthodiascopic 
tracing  of  a  broad  heart. 


may  amount  to  more  than  3  cm.  Another  factor  capable  of  producing 
wide  variations  from  the  standard  and  still  be  within  the  normal  is  that  of 
different  types  of  cardiac  contour  which  do  not  correspond  wTith  the  mus- 
cular make-up  of  the  individual.  The  extremes  are  those  with  long, 
slender,  graceful  hearts  scarcely  resting  upon  the  diaphragm,  and  those 
whose  hearts  are  broad,  lying  flat  along  almost  their  entire  lengths. 
For  example :  in  a  youth  of  19,  tall  and  slender  (Fig.  205)  M.R  =  3  cm. ; 
M.L  =  Q  cm. ;  the  other  is  the  orthodiagram  of  a  robust  male  of  35 
(Fig.  206).     Both  are  healthy  and  have  normal  hearts.     Marked  dif- 


114 


CLINICAL  CARDIOLOGY 


ferences  in  all  diameters  are  immediately  apparent  by  reference  to  the 
diagrams.  An  added  consideration,  already  alluded  to,  tending  to 
lessen  the  value  of  measurements  as  comparative  standards,  is  the  dif- 
ference produced  by  movements  of  the  diaphragm.  When  excursion 
of  the  latter  is  limited,  less  of  the  heart  is  uncovered,  its  ovoid  contour 
appears  flattened,  and  the  transverse  measurement  is  correspondingly 
enlarged.  With  a  mobile  diaphragm  the  reverse  is  usually  true.  From 
all  these  facts  it  is  apparently  impossible  to  establish  a  normal  mathe- 
matical  orthodiascopic   standard   of   measurement.     This    statement, 


Fig.  207. 


Fig.  208. 


Figs.  207,  208.  —  Orthodiascopic  tracings  of  abnormally  slender  hearts  resting  slightly  on 
the  diaphragm  (the  'drop'  heart). 

however,  does  not  preclude  such  general  conclusions  as  that  '  normal ' 
hearts  may  be  unusually  large  or  small,  or  that  pathologically  enlarged 
hearts  often  overstep  the  somewhat  ill-defined  normal  limits.  There  is 
naturally  no  doubt  of  the  value  of  orthodiascopy  in  the  determina- 
tion of  marked  variations  in  the  size  of  the  heart. 

The  Narrow  and  the  Broad  Heart.  —  Returning  to  a  discussion  of 
the  two  types  of  cardiac  silhouette  (Figs.  205,  206)  —  the  abnormally 
narrow  and  the  abnormally  broad  —  there  is  not  only  a  difference  in 
size  but  also  a  marked  difference  in  form.  The  left  ventricle  of  the  broad 
heart  is  flat,  lies  close  to  the  diaphragm,  and  forms  a  flattened  ovoid. 
The  other  type  is  ellipsoid,  and  rests  lightly  upon  the  diaphragm ;  Figs. 
207  and  208  are  additional  examples.  One  is  that  of  a  man  of  25  suffer- 
ing from  bronchial  asthma  (Fig.  207) ;   the  other  that  of  a  woman  of 


ORTHODIASCOPY  AND   FLUOROSCOPY 


115 


Fig.  209.  —  Orthodiascope  tracing  of  a 
woman  of  30  with  a  compensated  mitral 
regurgitant  lesion  showing  normal  cardiac 
contour  and  size. 


26  suffering  from  marked  vasomotor  symptoms  (Fig.  208).  This  type, 
sometimes  called  the  "  drop  heart,"  has  assumed  considerable  clinical 
importance,  for  it  has  been  found 
in  patients  with  visceroptosis,  is 
regarded  as  one  of  the  characteris- 
tics of  "  habitus  asthenicus,"  and 
is  apparently  the  type  of  cardiac 
hypoplasia  described  in  status 
thymolymphaticus.  The  symp- 
toms I  have  found  in  these  indi- 
viduals are  those  connected  with 
vasomotor  instability  —  flushes, 
pale  and  cold  extremities,  dizzi- 
ness, etc.  These  are  often  errone- 
ously interpreted  as  due  to  a 
'  weak  heart '  (Chapter  XX). 

Orthodiascopy  in  Mitral  Dis- 
ease. —  Orthodiascopy  has  been 
used  as  a  method  of  establishing 
the  diagnosis  of  valvular  lesions 
upon  the  assumption  that  these 
produce  typical  changes  in  cardiac 
contour.  With  reference  to  mitral  disease,  it  is  probably  true  that  many 
advanced  decompensated  patients  conform  in  a  general  way  to  an  or- 
thodiascopic  type,  but  those  with  quiescent  and  compensated  lesions 

may  possess  hearts  of  normal  size 
and  contour.  Two  illustrations  are 
given  in  Figs.  209  and  210.  The 
former  was  taken  from  a  woman 
of  30  with  a  mitral  regurgitant 
lesion  of  ten  years'  duration ;  the 
latter,  from  a  girl  of  17  with  a 
double  mitral  lesion  of  four  years' 
duration.  In  both,  there  were  typ- 
ical physical  signs  of  the  respective 
valvular  lesions ;  both  were  com- 
pensated, the  patient  with  the 
double  mitral  was  still  suffering 
from  rheumatic  manifestations  at 
the  time  the  orthodiagram  was 
taken.  Decompensated  double 
mitral  lesions  with  auricular  fibril- 
lation are  those  which  usually  con- 
form to  a  general  orthodiascopic 
type.  The  aorta  may  retain  its  normal  outline  or  be  somewhat  dilated, 
even  in  the  absence  of  physical  signs  of  an  aortic  lesion.     The  remainder 


Fig.  210.  —  Orthodiagram  of  a  girl  of  17 
with  a  compensated  double  mitral  lesion. 
The  tracing  is  normal  in  size  and  contour. 


116 


CLTNICAL  CARDIOLOGY 


ORTHODIASCOPY  AND   FLUOROSCOPY 


117 


of  the  cardiac  contour  forms  one  large  fused  outline  —  the  globular  heart 
('  Kugelherz  '),  consisting  of  the  dilated  pulmonary  artery,  left  auricular 
and  ventricular  curves  on  the  one  side,  and  a  ballooning  out  of  the  right 
auricular  curve  on  the  other. 
Figures  211,  212,  213  are  ex- 
amples showing  varying  degrees 
of  size  and  rotundity  of  outline 
from  three  cases  of  decompen- 
sated double  mitral  lesions  with 
auricular  fibrillation.  All  the 
patients  were  adults.  In  one 
(Fig.  211),  the  aortic  curve  is 
normal;  in  the  others,  it  is 
dilated.  Another  interesting 
example  of  the  globular  heart 
(Fig.  214)  is  the  orthodiagram 
of  a  boy  of  11  with  a  decom- 
pensated double  mitral  lesion 
and  auricular  fibrillation.  Oc- 
casionally, the  OrthodiasCOpic  Fig.  217.  —  Extreme  rounded  right-sided  en- 
trn pinery    of   nntipnt^   with    thp^p  largement.     The    left    contour  is   enlarged 

tracings    OI    patients    \\  ltn    tnese  downward.     From  a  case  of  double  mitral 

lesions      show     neither      extreme  lesion,  auricular  fibrillation,  and  cardiac  fail- 

enlargements     nor     a     definite        ure" 

rounded  outline,  thus :    Figure  215  is  the  tracing  of  a  man  of  50  who 

only  recently  developed  auricular  fibrillation ;   Fig.  216  is  from  a  woman 

of  46  who  has  had  the  valvular  lesion  and  arrhythmia  for  many  years. 

Other   variations  from  the  typical   globular  form   are  sometimes 

found  in  chronic  cases  of  double  mitral 
disease  with  fibrillation  in  which  there 
is  disproportionate  right-  and  left-sided 
enlargement.  For  example,  the  trac- 
ing in  Fig.  217  is  from  a  patient  of  35 
with  an  old  double  mitral  lesion,  fre- 
quently decompensated,  and  with  au- 
ricular fibrillation.  There  is  a  sharply 
rounded  right-sided  enlargement,  the 
left  side  is  enlarged  downwards  and 
outwards ;  the  resultant  silhouette  is 
an  irregular  ovoid. 

Of  great  interest  from  the  orthodia- 
scopic  standpoint  are  those  patients 
with  chronic  double  mitral  lesions 
without  auricular  fibrillation  in  whom 
there  has  never  been  any  severe  break  of  compensation.  The  trac- 
ings are  sometimes  normal  in  configuration  and  size,  as  in  a  case 
already  described  (Fig.  210),  or  the  enlargement  is  too  slight  to  be  of 


Fig.  218.  —  Copy  of  orthodiascope 
tracing  of  a  woman  of  55  with  a 
double  mitral  lesion  of  20  years'  dura- 
tion. There  is  only  very  slight  left- 
sided  enlargement. 


118 


CLINICAL   CARDIOLOGY 


Fig.  219.  —  Normal  orthodiascopic  tracing  of 
a  tall  boy  of  18  suffering  from  a  recent 
mitral  regurgitant  lesion. 


diagnostic  significance.  Thus,  a  woman  of  45  has  had  a  double  mitral 
lesion  over  twenty  years.  Recently  she  developed  occasional  extra- 
systoles  accompanied  by  a  sub- 
jective feeling  of  "  weakness  "  in 
the  chest.  Otherwise,  she  has 
never  had  any  cardiac  complaint. 
The  orthodiascopic  tracing  (Fig. 
218)  shows  only  very  slight  left- 
sided  enlargement. 

Regarding  the  orthodiagrams 
in  patients  with  mitral  regurgitant 
lesions,  there  may  be  no  abnormal 
change  of  cardiac  outline,  particu- 
larly when  the  lesions  are  recent 
and  quiescent,  or  are  fully  com- 
pensated. One  example  has  been 
mentioned  above  (Fig.  209). 
Another  instance  is  the  tracing  of 
a  tall,  well-built  lad  of  18  (Fig. 
219),  who  recently  recovered  from  the  acute  manifestations  of  mild 
rheumatic  mitral  regurgitation. 

In  chronic  mitral  regurgitation  with  decompensation,  the  orthodia- 
scopic tracing  is  usually  ovoid  or  somewhat  circular  in  shape.  The 
longest  axis  lies  diagonally,  the 
larger  end  corresponding  to  the  left 
ventricle.  The  elements  constitut- 
ing the  abnormal  form  are  moder- 
ate enlargement  of  the  left  auricu- 
lar, ventricular,  and  the  right 
auricular  curves.  An  instance  of 
this  is  seen  in  Fig.  220,  a  female 
aged  35  with  a  rheumatic  mitral 
regurgitant  lesion;  the  orthodia- 
gram shows  an  ovoid  heart  with 
moderate  dilatation  of  the  left 
border.  If  decompensation  is  ex- 
treme, the  entire  contour  becomes 
circular. 

Orthodiascopy  in  Rheumatic 
Aortic  Disease.  —  With  reference 
to  rheumatic  lesions  of  the  aorta, 
one  of  the  chief  fluoroscopic  char- 
acteristics is  the  degree  of  the  aortic 
excursion,  the  aortic  fling.  This  is 
observed  in  patients  with  double  aortic  lesions  whether  compensated 
or  not.     As  a  rule,  the  aorta  itself  is  not  permanently  enlarged,  although 


Fig.  220.  —  Orthodiagram  of  a  woman  of 
35  with  a  mitral  regurgitant  lesion  show- 
ing a  somewhat  ovoid  contour  with 
moderate  dilatation  to  the  left. 


ORTHODIASCOPY  AND  FLUOROSCOPY 


119 


Fig.  221.  —  Typical  orthodiagram  of 
old  rheumatic  double  aortic  lesion. 
From  a  woman  of  45  showing  ex- 
treme left  ventricular  enlargement 
and  dilatation  of  the  first  part  and 
arch  of  the  aorta. 


this  impression  is  gained  from  the  occasional  violent  systolic  expansion. 
There  appears  to  be  some  relation  between  the  clinical  severity  of  the 
disease  as  gauged  by  the  dyspnoea  and  cardiac  reserve  power,  and  the 
degree  of  aortic  fling.  In  cases  severely 
ill,  the  entire  aorta,  the  ascending,  arch, 
and  descending  portions  pulsate  so 
violently  as  to  resemble  an  aneurism ; 
those  less  ill  usually  show  excursion 
limited  to  individual  sections  of  this 
vessel.  Another  fluoroscopic  character- 
istic of  aortic  lesions  is  the  sharp,  vigor- 
ous left  ventricular  contraction,  with  a 
distinct  lifting  motion  of  the  apical 
region.  When  left  ventricular  hyper- 
trophy is  extreme,  the  contraction  of  the 
apical  region  is  so  marked  as  to  appear 
separate  from  the  remainder  of  the  left 
ventricle.  In  general,  it  may  be  stated 
that  the  ventricular  excursion  during 
systole  is  greater  in  aortic  valvular  lesions  than  in  the  other  types  of 
cardiac  disease ;  this  is  sometimes  of  diagnostic  significance  in  suspected 
aortic  disease  with  indistinct  and  atypical  clinical  signs. 

The  change  in  cardiac  contour  found  in  aortic  valvular  lesions  is 

more  constant  than  in  mitral  dis- 
ease. The  apical  region  is  enlarged 
and  obtuse,  and  the  apex  itself  is 
often  found  near  the  axillary  line. 
The  body  of  the  left  ventricle  is 
egg-shaped.  The  right  auricular 
curve  is  moderately  increased  in 
convexity,  the  entire  auriculo-ven- 
tricular  outline  presents  an  abnor- 
mally broadened,  flat,  somewhat 
egg-shaped  oval,  with  the  wide  end 
at  the  apex.  In  conjunction  with 
the  curves  formed  by  the  aorta 
and  pulmonary  artery,  the  entire 
cardiac  outline  roughly  resembles 
the  "  duck-shaped  heart "  de- 
scribed by  Groedel. 

Several  typical  illustrations  of 
double  aortal  lesions  follow : 

Figure  221  is  the  orthodiagram 
of  a  woman  of  55  with  an  old  rheumatic  history.  There  was  dilatation 
of  the  first  part  and  arch  of  the  aorta.  The  entire  left  ventricle  was 
greatly  hypertrophied,  its  outlines  enlarged,  the  pulmonary  curve  flat- 


Fig.  222.  —  Orthodiagram  of  a  patient  with 
aortic  regurgitation.  From  a  boy  of  19, 
showing  left  ventricular  hypertrophy  and 
moderate  enlargement  of  the  aortic  arch. 
The  pulmonary  and  left  auricular  curves 
are  small. 


120 


CLINICAL  CARDIOLOGY 


tened,  the  left  auricular  curve  very  small.  Fluoroscopically,  there  was 
very  marked  aortal  fling  of  the  entire  visible  aorta. 

Figure  222  is  the  tracing  of  a  boy  of  19  with  a  rheumatic  aortic  lesion 
of  twelve  years'  duration.  There  was  marked  left  ventricular  hyper- 
trophy, the  pulmonary  and  left,  auricular  curves  were  small,  there  was 
moderate  dilatation  of  the  aortic  arch ;  fairly  marked  aortal  fling  was 
present.  "Whether  the  right-sided  enlargement  was  due  to  the  right 
auricle  itself,  or  whether  an  enlarged  left  ventricle  pushed  the  right 
auricle  abnormally  to  the  right,  was  not  clear. 

While  the  entire  foregoing  description  applies  especially  to  double 
aortic  lesions,  with  some  differences  it  also  applies  to  aortic  stenosis 
alone.  In  the  latter  the  size  and  shape  are  similar  to  the  former,  but 
enlargement  of  the  various  curves  is  not  so  extreme,  and  the  aortic 
fling  is  not  as  marked. 

Orthodiascopy  in  Combined  Aortic  and  Mitral  Disease. — In  com- 
bined aortic    and   mitral   lesions,  the  orthodiascope   tracing   usually 


Fig.  224. 


Figs.  223,  224.  —  Orthodiagrams  of  two  cases  of  double  mitral  and  aortic  lesions.  The 
outlines  are  characteristic  of  the  latter  in  Fig.  224.  Fig.  223  is  not  characteristic  of 
either  lesion. 

follows  the  type  of  the  one  clinically  predominant.  Thus,  Figs.  223 
and  224  are  taken  from  two  cases  of  mitral  regurgitation  and  double 
aortic  lesion.  The  first  is  that  of  a  girl  of  12  in  whom  endocarditis 
developed  at  the  age  of  5 ;  the  second,  that  of  a  girl  of  19,  the  duration 
of  whose  endocarditis  is  not  known.  The  first  is  not  characteristic  of 
either  lesion;  the  second  shows  the  characteristics  of  aortic  lesions 
from  which  this  patient  chiefly  suffered. 


Orthodiascopy  in  Aortitis 

Aortitis  with  secondary  involvement  of  the  aortic  cusps  belongs  in 
a  different  category  from  the  rheumatic  valvular  lesions.     Although 


ORTHODIASCOPY  AND   FLUOROSCOPY 


121 


calcification  and  thickening  of  the  aorta  do  not  necessarily  imply  en- 
largement and  dilatation,  the  latter  is  the  rule  in  aortitis.  This  lesion 
may  be  confined  to  the  first  part 
(the  ascending  aorta),  to  the 
arch,  or  to  the  descending  tho- 
racic aorta ;  or  may  involve  the 
entire  thoracic  and  even  part  of 
the  abdominal  aorta.  Hence, 
it  is  important  to  distinguish 
aneurismal  dilatations  and  en- 
largements of  various  parts  of 
this  vessel. 

Moderate  dilatation  and  en- 
largement of  the  first  or  ascend- 
ing part  of  the  aorta  are  char- 
acterized by  an  abnormally 
broad  shadow  which  originates 
below  the  normal  level.  The 
left  border  of  the  arch  is  found 
beyond  its  usual  limits  and,  in 
addition,  may  be  sharply  curved.  The  entire  aortal  shadow  thus  be- 
comes abnormally  broad.  This  type  of  enlargement  accompanies 
aortitis  from  any  cause  —  senile  arteriosclerosis,  chronic  nephritis  with 

hypertension,  luetic  aortitis;   it  is  rarely 
found  in  rheumatic  aortic  valvular  dis- 


Fig.  225.  —  Dilatation  of  the  aortal  arch ;  left 
ventricular  hypertrophy.  From  a  male  patient 
of  45  with  chronic  nephritis  and  moderate  hy- 
pertension. 


ease. 


As  with  standard  of  measurements  for 
the  cardiac  orthodiagram,  similarly  there 
are  several  objections  to  a  standard  meas- 
urement for  the  normal  aorta.  Some  of 
these  are  the  indefinite  point  of  origin  of 
the  aorta,  the  difficulty  at  times  of  delim- 
iting its  borders,  the  high  or  low  posi- 
tion of  the  arch,  the  size  and  shape  of  the 
heart  of  each  individual.  In  aortic  dila- 
tation of  moderate  degree,  the  diagnosis 
may  therefore  depend  upon  abnormal 
contour  rather  than  upon  abnormal  size 
of  the  vessel.  In  moderate  dilatation  of 
the  ascending  aorta  there  is  a  slight  out- 
ward ballooning  of  the  right  aortal  out- 
line ;  in  that  of  the  arch,  the  curve  is 
broadened ;  in  that  of  the  descending 
part  of  the  arch,  there  is  distinct  widening  of  the  entire  aorta.  Finally, 
there  are  dilatations  confined  to  the  descending  thoracic  aorta ;  the 
latter  then  assumes  a  spindle-like  or  diffuse  enlargement,  which  lies 


Fig.  226.  —  Aortitis  with  enlarge- 
ment of  the  first  portion  and  arch 
of  the  aorta,  and  left  ventricular 
dilatation.  From  a  patient  of  65 
with  symptoms  of  general  arterial 
sclerosis  appearing  one  year  after 
a  very  severe  grippe  infection. 


i22 


CLINICAL   CARDIOLOGY 


mainly  behind  the  ventricles.  The  various  types  of  aortic  enlargement 
are  sometimes  best  seen  and  recognized  by  turning  the  patient  in  differ- 
ent directions  in  order  to  obtain  lateral  and  diagonal  views  of  the  aorta. 

This  is  of  particular  value  in  differ- 
entiating aortal  shadows  from  other 
structures;  for  example,  from  tu- 
mors, which  in  a  sagittal  direction 
simulate  the  aorta  in  area  and  po- 
sition. 

Orthodiagrams  of  various  types 
and  degrees  of  aortitis  with  ac- 
companying cardiac  hypertrophy 
and  of  aneurismal  dilatations  are 
shown  in  Figs.  225-232,  Fig. 
233  (Plate  XIX),  Fig.  234  (Plate 
XX),  Fig.  235,  with  a  brief  sum- 
Fig.  227.  —  Dilatation  of  the  aortal  arch  and    mary  of  their  etiology  and  clinical 

left    ventricular    hypertrophy.     From    a     diagnosis. 
patient  of  60  with  arteriosclerosis.  & 


Congenital  Cardiac  Malformations 

Aortic  stenosis  is  one  of  the  more  frequent  congenital  malformations. 
It  usually  occurs  about  2\  cm.  above  the  implantation  of  the  aortal 
cusps  and  constricts  the  vessel  to  a  varying  degree.  It  may  be  the 
only  congenital  cardiac  anomaly.  As 
in  other  congenital  defects  of  the 
heart,  the  patients  during  childhood 
or  adolescence  often  develop  endo- 
carditis of  the  aortic  or  other  valves, 
conditions  which  partially  or  entirely 
mask  the  stenosis. 

The  following  are  brief  reports  of 
cases  with  orthodiagrams  of  the  fore- 
going congenital  defect : 

A  male,  age  21  years,  had  had  a 
very  severe  attack  of  scarlet  fever 
when  10  years  old  ;  it  was  followed  by 
endocarditis  affecting  the  mitral  and 
aortal  valves.  The  patient  was  then 
abed  for  several  months.  Except  for 
occasional  attacks  of  hematuria,  he 
felt  quite  well  until  his  twenty-first 
year.  At  that  time  he  complained  of  lassitude  for  several  weeks, 
during  which  there  were  no  rheumatic  manifestations  or  fever.  Upon 
examination,  the  heart  was  found  enlarged  to  the  left;  there  was 
an  area  of  dullness  over  the  second  and  third  right  interspaces  where  a 


Fig.  228.  —  Aortitis  of  the  first  portion 
and  arch  of  the  aorta,  and  extreme  left 
ventricular  hypertrophy.  From  a  man 
of  50  with  cardiosclerosis  and  decom- 
pensation. The  first  clinical  symp- 
toms occurred  six  months  after  a  very 
severe  streptococcus  pneumonia. 


PLATE   XIX 


^1 

■ ...  ,  ■  ■ 

fc-fc          ^?At  -^ 

BjW^P^^H 

|^^^^(B 

1 

•:-,.                                                                                       ^ 

Wf           ^^H 

W                         ^^^1 

HEl                         ^|hl   J 

Hr 

1 

j^^H 

• 

Fig.  233.  — Photograph  from  X-ray  plate,  showing  aneurysmal  dilation  of  the  descending 

thoracic  aorta. 


PLATE   XX 


Fig.  234.  —  Photograph  from  Roentgenogram  of  aneurismal  dilatation  of  the  descending 
thoracic  aorta ;  marked  left  ventricular  hypertrophy.  From  a  woman  of  50  with  a 
positive  Wassermann  reaction  of  the  blood. 


ORTHODIASCOPY  AND   FLUOROSCOPY 


123 


loud  systolic  and  a  fainter  diastolic  murmur  were  heard.  There  was 
also  the  auscultatory  evidence  of  a  double  mitral  lesion.  The  Wasser- 
mann  blood  reaction  was  negative.  Fluoroscopic  examination  showed 
aneurism  of  the  first  portion  of  the  aorta  (Fig.  235).     The  diagnosis  of 


Fig.  229.  —  Luetic  aortitis  affecting  the    Fig.  230.  —  Enlargement  and  low  implantation 


arch.  Left  ventricular  hypertrophy 
From  a  patient  of  60  with  a  luetic  his- 
tory and  a  positive  Wassermann  blood 
reaction. 


of  the  first  portion  of  the  aorta ;  moderate 
enlargement  of  the  left  ventricle.  From  a 
male  patient  of  58  with  chronic  nephritis  and 
myocarditis. 


congenital  aortic  stenosis  was  made.  Some  weeks  later,  the  patient 
developed  acute  gastric  symptoms  with  fever.  A  tentative  diagnosis 
of  streptococcus  viridans  infection  was  made ;  this  was  confirmed  two 
days  later  by  positive  blood  culture.  Despite  immediate  treatment 
with  autogenous  vaccines  and  sen- 
sitized horse  serum,  the  patient 
died  within  a  few  months.  At 
necropsy,  the  mitral  and  aortic 
cusps  were  found  encrusted  with 
granulomatous  masses,  some  of 
which  were  imbedded  in  the 
sinuses  of  Valsalva.  There  was 
moderate  congenital  constriction 
of  the  aorta  3  cm.  above  the 
cusps.  There  were  no  other  con- 
genital maformations.  It  is  of 
great  interest  to  note  that  though 
serum  therapy  was  begun  within 
a  very  few  days  after  the  onset  of 
the  acute  symptoms  and  was  systematically  continued,  there  was  abso- 
lutely no  evidence  at  necropsy  that  the  progress  of  the  disease  had  in 
any  wise  been  checked. 

A  woman,  aged  51,  had  scarlet  fever  when  6  and  "heart  disease" 


Fig.  231.  —  Luetic  aortitis  affecting  the  arch ; 
left  ventricular  hypertrophy. 


124 


CLINICAL  CARDIOLOGY 


when  7  years  old.  From  that  time  until  the  present,  she  has  had  fre- 
quent attacks  of  decompensation.  From  her  account,  she  appears  to 
have  had  attacks  of  paroxysmal  tachycardia;    otherwise,  the  pulse 

had  been  regular  until  quite  re- 
cently. She  then  developed  rapid 
and  irregular  heart  action,  orthop- 
ncea  and  anasarca.  The  electro- 
cardiogram revealed  auricular 
fibrillation;  there  was  definite 
auscultatory  evidence  of  a  double 
mitral  lesion.  At  the  first  exami- 
nation, the  sounds  at  the  right  base 
appeared  normal.  With  the  res- 
toration of  compensation  and  de- 
crease of  the  ventricular  rate,  a  soft 
systolic  and  a  fainter  diastolic 
murmur  were  heard  over  the  right 
base ;  there  were  no  additional 
signs  of  an  aortic  lesion.  Fluoro- 
scopic examination  showed  a  large 
pulsatile  enlargement  of  the  first 
portion  of  the  aorta  (Fig.  237).  From  the  history  and  fluoroscopic  find- 
ings, it  seems  most  probable  that  the  aortic  enlargement  was  due  to 
congenital  aortic  stenosis. 


Fig.  232.  —  Diffuse  aneurismal  dilatation  of 
the  descending  thoracic  aorta.  From  a 
patient  of  69  with  a  history  of  a  luetic  in- 
fection 40  years  ago,  and  a  positive  Was- 
sermann  reaction  of  the  blood. 


Patent  Ductus  Arteriosus  or  Ductus  Botalli 

This   congenital  defect  is   not  rare.     Cardiac  symptoms   are  not 
always  present ;   when  they  are,  the  usual  history  is  that  the  patients 


Fig.  235.  —  Aneurismal   dilatation  of  the 
arch  and  descending  thoracic  aorta. 


Fig.  236.  —  Aneurism  of  the  first  portion  of 
the  aorta  due  to  congenital  aortic  stenosis. 


were  born  cyanotic.  The  cyanosis  is  increased  by  crying,  by  exposure 
to  cold,  and,  in  older  children,  by  exertion  and  exercise.  Upon  per- 
cussion, a  slight  extension  of  cardiac  dullness  in  the  second  left  inter- 


ORTHODIASCOPY  AND   FLUOROSCOPY 


125 


Fig.  237.  —  Orthodiagram  of  a  patient  with 
a  double  mitral  lesion  and  aortic  aneurism, 
the  latter  probably  due  to  congenital  aortic 

[stenosis. 


space  (Gerhardt's  area  of  dullness)  can  sometimes  be  mapped  out.  A 
rough  systolic  thrill  is  felt,  and  a  loud,  rough  systolic  murmur  is  heard, 
most  intensely  over  this  area.  The  murmur  is  usually  transmitted 
over  the  entire  precordium  and 
into  the  carotids.  In  addition, 
there  is  sometimes  a  loud  diastolic 
murmur  most  prominent  in  the 
left  upper  interspaces  near  the 
sternum ;  the  double  murmur 
thus  produced  is  called  a 
"  machinery  murmur."  The 
presence  and  intensity  of  the  dia- 
stolic murmur  apparently  depend 
upon  the  amount  of  blood  which 
regurgitates  through  the  patent 
duct,  and,  in  its  mechanism,  re- 
sembles aortic  insufficiency;  in- 
deed, capillary  pulsation  has  been 
described  as  an  occasional  ac- 
companiment of  this  lesion.  The 
orthodiascopic  picture  in  typical 
cases  of  patent  ductus  arteriosus 
is  that  of  a  vigorously  pulsating 
aortic  arch  increased  in  size,  beneath  which  is  found  an  enlarged,  flat- 
tened, or  protuberant  overacting  pulmonary  artery.  The  duct  itself  is 
rarely  visible  because  of  its  small   size  and  frequent  involvement  in 

pericardial  adhesions.  The  latter  was 
found  in  two  autopsy  specimens  I  have 
seen. 

The  following  is  an  illustrative  his- 
tory, with  clinical  and  orthodiascopic  find- 
ings, of  a  patient  with  patent  ductus 
Botalli.  Male,  age  16,  tall  and  spare, 
was  born  a  "  blue  baby."  He  had 
scarlet  fever  when  seven  years  old.  He 
had  never  been  able  to  play  actively  or 
to  run.  He  frequently  complains  of 
palpitation ;  he  has  a  productive  cough 
and  has  had  hemoptyses.  His  face  and 
extremities  are  cyanotic,  his  lips  almost 
black,  his  fingers  markedly  clubbed. 
There  are  vigorous  carotid  and  jugular 
pulsations  and  a  strong  visible  ventricu- 
lar impulse ;  the  apex  is  most  prominent  in  the  fifth  interspace.  A  strong 
systolic  pulsation  is  seen  in  the  second  and  third  left  interspaces  just  out- 
side the  sternal  border.     There  is  a  marked  palpable  carotid  thrill  felt 


Fig.  238.  —  Orthodiagram  of  a  boy 
of  16  with  patent  ductus  arteri- 
osus. The  curve  of  the  pulmo- 
nary artery  (P. A.)  is  extremely 
enlarged  and  flattened. 


126  CLINICAL  CARDIOLOGY 

almost  up  to  the  angle  of  the  jaw.  There  is  also  a  rough  thrill  most 
prominent  in  the  second,  third,  and  fourth  left  interspaces,  less  marked 
in  the  second  and  third  right  interspaces.  A  definite  "  Gerhardt's  area 
of  dullness  "  can  be  mapped  out  by  percussion.  Upon  auscultation,  a 
loud  systolic  murmur  is  heard  over  the  entire  precordium,  and  over 
the  chest  posteriorly.  The  murmur  is  especially  loud  and  rasping  over 
the  second  and  third  left  interspaces  and  over  the  manubrium  sterni. 
The  fluoroscope  reveals  a  vigorously  overacting  aorta  and  pulmonary 
artery;  the  latter  is  extremely  enlarged  and  flattened  (Fig.  238).  The 
electrocardiogram  shows  a  negative  R  deviation  in  the  first  and  second 
leads,  an  evidence  of  right  ventricular  preponderance. 

Patent  Interventricular  Septum 

This  congenital  anomaly  is  extremely  uncommon  and  very  rarely 
exists  as  an  isolated  defect.  Cyanosis  is  the  most  prominent  clinical 
sign ;  its  degree  depends  upon  the  size  of  the  interventricular  aperture, 
and  upon  the  presence  of  other  congenital  defects  —  usually  pulmonary 
atresia.  The  extremities  are  clubbed,  there  is  a  marked  coarse  systolic 
thrill  to  be  felt,  and  a  corresponding  rough  murmur  to  be  heard,  over 
the  entire  precordium ;  the  maximum  intensity  of  the  murmur  and  thrill 
is  over  the  xiphoid  and  epigastrium.  There  is  also  vigorous  epigastric 
pulsation.  In  the  orthodiagram  the  left  auricle  and  ventricle  are 
hugely  dilated  and  rounded,  the  heart  is  also  enlarged  to  the  right; 
because  of  atresia  of  the  pulmonary  artery  its  pulsation  may  be  slight 
or  absent. 

A  unique  instance  of  patent  interventricular  septum  in  a  child  with 
congenital  dextrocardia  came  under  my  observation.  The  history 
follows : 

A  male,  age  3f  years,  was  the  youngest  of  nine  children;  he  had 
measles  and  pertussis  when  two  years  old.  The  mother  said  the  child 
had  always  been  "  blue  "  and  "  short  of  breath,"  but  never  sufficiently 
dyspnceic  to  be  bedridden.  The  child  appears  well  nourished.  The 
extremities,  lips,  face,  and  conjunctivae  are  cyanosed  ;  the  conjunctival 
blood  vessels  are  congested ;  there  is  distention  of  the  superficial  veins 
of  the  chest  and  abdomen.  The  fingers  and  toes  are  clubbed.  There 
is  a  vigorous,  heaving  systolic  impulse  in  the  right  axillary  line  and 
in  the  epigastrium.  A  strong,  marked  systolic  thrill  can  be  felt  over 
the  entire  precordium;  it  is  roughest  and  most  prominent  at  the 
lower  end  of  the  sternum  and  in  the  epigastrium.  Over  the  former 
there  is  a  loud,  rough  systolic  murmur  becoming  fainter  over  the 
remainder  of  the  chest,  anteriorly  and  posteriorly.  It  is  also  trans- 
mitted along  the  carotids.  There  is  no  Gerhardt's  area  of  dullness 
in  the  second  and  third  right  interspaces.  The  liver  and  spleen  are 
not  transposed ;  the  gastro-intestinal  canal,  as  shown  by  bismuth 
roentgenograms,  is  in  its  normal  position.     Fluoroscopy  of  the  chest 


ORTHODIASCOPY  AND   FLUOROSCOPY 


127 


reveals  an  enlarged  and  vigorously  pulsating  aorta.  Beneath  it,  the 
usual  pulsating  curve,  representing  the  pulmonary  artery,  is  absent. 
In  its  stead,  there  is  a  tremendously  di- 
lated, prominent,  and  knob-like  '  left '  l 
auricle.  The  '  left '  ventricular  shadow  is 
also  very  much  enlarged  ;  its  area  cannot 
be  definitely  separated  from  the  superim- 
posed auricle,  although  their  non-syn- 
chronous pulsations  can  be  readily  deter- 
mined. The  '  right '  auricle  is  enlarged  ; 
beneath  it,  the  beginning  of  the  '  right 
ventricular  '  shadow  is  seen  deeply  depress- 
ing the  diaphragm  during  inspiration. 
From  this  finding,  it  is  probable  that  the 
'  right '  ventricle  is  enlarged.  The  ortho- 
diagram (Fig.  239)  showed  a  greatly  di- 
lated aorta,  rounded  and  prominent,  and 
coalescence  of  the  '  left '  auricular  and 
ventricular  curves.  The  '  right  auricular  ' 
curve  is  also  considerably  enlarged.  The 
electrocardiogram  shows  the  typical  down- 
ward deviation  of  the  P,  R,  and  T  waves 
in  the  first  lead,  pathognomonic  of  con- 
genital dextrocardia.  A  diagrammatic  representation  of  the  probable 
circulation  in  this  case  is  also  shown  in  Fig.  240. 


Fig.  239.  —  Orthodiagram  of  a 
child  with  congenital  dextro- 
cardia and  patent  interventric- 
ular septum.  It  shows  an  en- 
larged and  broadened  aortal 
curve  and  enlarged  '  right ' 1 
auricular  curve,  coalescence  of 
enlarged  and  knob-like  left  au- 
ricular and  ventricular  curves, 
and  absence  of  pulmonary  promi- 
nence. 


Fig.  240.  —  Diagram  of  probable  car- 
diac circulation  in  the  patient  DL 
Solid  arrows  =  main  circulation 
Dotted  arrows  =  minor  circulation 

R.A      =  right  auricle ; 

R.V      —  right  ventricle; 

L.A      =  left  auricle  ; 

L.V      =  left  ventricle; 

P.D.A  =  patent  ductus  arteriosus ; 

P.C      =  pulmonary  circulation  ; 

S.P.A  =  stenosed  pulmonary  artery 


Patent  Foramen  Ovale 

When  present  as  an  isolated  anom- 
aly, and  of  only  moderate  size,  this 
interauricular  septal  defect  rarely  pro- 
duces clinical  signs  or  diagnostic  symp- 
toms. As  proven  at  necropsy,  patients 
with  even  large  defects  have  presented 
during  life  no  signs,  clinical  or  other- 
wise, upon  which  a  correct  diagnosis 
might  have  been  based.  Cyanosis  is 
rarely  present ;  occasionally,  systolic  or 
diastolic  murmurs  are  heard  over  the 
third  left  interspace.  Orthodiascopic 
tracings  present  nothing  characteristic. 


1  To  avoid  confusion  in  the  description 
of  this  case  of  congenital  dextrocardia, 
'  left '  and  '  right '  are  used  in  the  sense  as 
usually  applied  to  the  normal  heart  in  its  normal  position  ;  that  is, '  left '  will  re- 
fer to  the  larger,  and  '  right '  to  the  smaller  ventricle  with  its  corresponding 
auricle. 


128  CLINICAL  CARDIOLOGY 

Of  congenital  lesions  in  general,  it  may  be  broadly  stated  that  patients 
with  a  single  congenital  defect  are  those  who  are  most  apt  to  survive 
and  reach  adult  life.  If  more  than  one  congenital  anomaly  is  present, 
the  chances  for  longevity  are  correspondingly  diminished. 

REFERENCES 

Chapteb  IX 

Dietlin,  H.  :  Ueber  Groesse  und  Lage  des  normalen  Herzens  und  ihre  Abhaengig- 
keit  von  phvsiologischen  Bedingungen  ;  23ten  Kongress  fuer  innere  Medizin, 
1906,  267. 

Emerson,  H. :  Status  Lymphaticu s  in  Adults,  Its  Clinical  Diagnosis  and  Im- 
portance ;  Archives  of  Internal  Medicine,  1914,  XIII,  169. 

Groedel,  F.  M. :  Die  Roentgendiagnostik  der  Herz-  und  Gefaesskrankheiten. 

Moffatt,  R.  D.,  and  Neuhof,  S. :  Congenital  Dextrocardia  with  Patent  Inter- 
ventricular Septum  ;  American  Journal  of  Diseases  of  Children,  1915,  X,  1. 

Norris,  C. :   On  Status  Lymphaticus ;  Johnson's  Surgical  Diagnosis,  III,  705. 

Veith,  A. :  Ueber  orthodiagraphische  Herzuntersuchungen  bei  Kindern,  etc. ; 
Jahrbuch  fuer  Kinderheilkunde,  1908,  LXVIII,  268. 


CHAPTER  X 
PHYSICAL  EXAMINATION   OF   THE   HEART 

Ea.ch  of  the  usual  methods  of  clinical  examination  —  inspection, 
palpation,  percussion,  and  auscultation  —  yields  valuable  information 
in  appropriate  cases.  Ordinarily,  most  emphasis  is  placed  upon  auscul- 
tation and  percussion,  less  upon  inspection  and  palpation.  In  my 
opinion  the  latter,  though  frequently  neglected  as  routine  methods  of 
examination,  are  often  of  diagnostic  and  prognostic  importance.  Least 
valuable  and  most  deceptive  of  all  methods  is  information  gained  by  per- 
cussion. 

Inspection 

Inspection  of  the  chest  and  neck  frequently  reveals  important 
data  concerning  the  cardiovascular  system. 

Jugular  Pulsation.  —  The  manner  of  filling,  and  the  degree  of  dis- 
tention, of  the  jugular  veins  is  best  observed  by  placing  the  patient  in 
the  supine  position.  Even  pulsation  of  the  thyroid  veins  may  be  visible. 
In  patients  with  long-continued  decompensation  it  is  common  to  find 
the  jugular  veins  tortuous,  thickened,  engorged,  and  greatly  distended ; 
the  situation  of  the  valves  is  particularly  prominent.  These  evidences 
of  chronic  venous  stasis  are  especially  marked  in  old  mitral  stenotic 
lesions  with  auricular  fibrillation,  or  in  old  patients  with  decompensated 
cardiosclerosis.  Tricuspid  regurgitation  from  relative  insufficiency  or 
valvular  disease  is  sometimes  accompanied  by  engorged  or  hyperactive 
pulsatile  jugulars,  although,  as  already  mentioned,  the  interposition  of 
the  right  auricle  probably  prevents  such  jugular  hyperaetion  in  many 
instances.  In  cases  of  auricular  extrasystoles,  the  premature  jugular 
pulsation  {a'  wave)  may  occasionally  be  visible.  More  often,  the 
coincidence  of  auricular  and  carotid  waves  (composite  a'  +  c'  wave, 
Chapter  VII)  found  in  ventricular  extrasystoles  is  recognized  in  the 
jugulars  as  abnormally  large  and  premature  pulsations.  A  similar 
jugular  wave,  not  premature  in  the  time  of  its  occurrence,  is  present  in 
complete  heart  block  when  auricles  and  ventricles  beat  synchronously 
(a-f-cwaves;  Chapter  VII,  Heart  Block).  This  observation  is  of  use 
in  the  differentiation,  by  inspection,  between  complete  and  incomplete 
heart  block,  for  in  the  latter  there  are  no  such  superimposed  waves.     In 

K  129 


130  CLINICAL  CARDIOLOGY 

auricular  flutter,  the  jugular  pulsations  are  usually  too  faint  and  indis- 
tinct to  be  counted ;  however,  in  one  case  that  I  observed  the  jugular 
veins  literally  throbbed,  and  were  so  engorged  that  the  number  of 
pulsations  could  be  clearly  discerned  at  a  distance  of  several  feet.  In 
auricular  fibrillation,  in  addition  to  the  distention  already  referred  to, 
the  jugulars  beat  irregularly  in  consonance  with  the  arrhythmic  c-v 
waves. 

The  Carotid  Pulse.  —  The  inspection  of  the  carotid  pulse  is  of  great 
importance.  By  its  vigor,  overaction,  and  pulsatile  distention,  it  is 
often  indicative  of  aortal  disease  or  of  hypertension ;  if,  in  addition, 
the  carotids  visibly  and  markedly  collapse  with  diastole,  they  indicate 
an  aortic  regurgitant  lesion.  Vigorously  throbbing  carotids  also  ac- 
company rapid  and  violent  heart  action  from  any  cause  (for  example, 
exophthalmic  goiter).  But  visible  carotid  hyperaction  with  a  normal 
pulse  rate  in  the  middle  aged  or  the  old  is  usually  evidence  of  aortitis 
or  of  hypertension ;  its  absence,  however,  does  not  necessarily  exclude 
these  conditions.  This  type  of  carotid  action  is  also  seen,  though 
rarely,  in  young  individuals  with  normal  hearts ;  in  them,  it  often 
corresponds  to  strong  systolic  ventricular  contractions  which  can  be 
very  readily  observed  by  fluoroscopic  examination. 

Aortic  Pulsation.  — Allied  to  carotid  overaction  in  clinical  significance 
is  aortic  pulsation,  recognized  by  the  pulsatile  rise  of  the  tissues  in 
the  jugulum.  This  indicates  more  advanced  aortal  changes  than  does 
carotid  overaction  alone.  Aortic  expansion  is  most  noticeable  in  aortic 
regurgitation  with  left  ventricular  hypertrophy,  and  in  aneurisms  and 
aneurismal  dilatation  of  various  parts  of  the  aorta,  especially  during 
the  stage  of  decompensation.  On  the  chest  wall,  capillary  pulsation 
characteristic  of  aortic  regurgitation  may  occasionally  be  seen.  A 
band  of  dilated  venules  and  capillaries  over  the  lower  anterior  part  of 
the  chest  sometimes  accompanies  aortic  lesions,  particularly  aneurisms 
or  aneurismal  dilatations.  Large  aneurisms  that  touch,  adhere  to,  or 
erode  the  chest  wall  naturally  give  rise  to  visible  pulsatile  expansion; 
their  usual  site  is  the  second  and  third  right  interspaces  and  the  inter- 
clavicular notch,  more  rarely  the  left  upper  interspaces.  Aneurismal 
dilatations  of  the  aorta  are  rarely  adherent  and  very  infrequently  cause 
erosion.  If  they  touch  or  approach  the  chest  wall,  pulsatile  expansion, 
otherwise  not  noticeable,  may  be  seen  by  placing  the  eye  on  a  level 
with  the  chest.  By  this  method,  not  only  dilatations  of  the  first  part 
and  arch,  but  even  aneurismal  dilatation  of  the  descending  thoracic 
aorta  (Chapter  XIV)  may  be  discerned  as  a  distinct  and  separate  systolic 
heave  above  and  partly  behind  the  rise  of  the  left  ventricle. 

Inspection  of  the  Apical  Region.  —  Regarding  the  apical  and  pre- 
cordial region,  important  information  can  be  gleaned  by  inspection 
alone.  In  thin-chested  individuals  with  decompensated  mitral  stenosis, 
it  is  often  possible  to  discern  an  overacting  pulmonary  artery  which, 
upon  auscultation,  produces  an  accentuated  and  clicking  second  sound. 


PHYSICAL  EXAMINATION   OF  THE   HEART  131 

Many  varieties  of  abnormal  ventricular  action  are  also  readily  recognized 
by  inspection.  Thus  ventricular  activity  is  visible  over  almost  the 
entire  precordium  in  massive  left  ventricular  hypertrophy,  in  the  violent 
action  of  tachycardia,  in  the  ventricular  dilatation  of  the  acute  stages  of 
valvular  endocarditis,  or  in  some  congenital  lesions.  An  overacting 
ventricular  impulse  may  be  confined  to  a  small  area  at  the  apex  in  mitral 
lesions,  especially  in  young  individuals.  One  often  finds  heaving,  broad 
ventricular  impulses  in  old,  decompensated  mitral  lesions.  Obviously, 
the  thickness  of  the  chest  wall,  the  posture  of  the  patient,  and  the 
illumination  are  considerations  which  considerably  mask  or  influence 
these  physical  data.  In  thin-chested  individuals,  or  in  women  with  the 
left  breast  well  raised,  it  is  sometimes  possible  to  distinguish  a  double 
systolic  impact  corresponding  to  the  reduplicated  first  sound  (q.v.)  heard  on 
auscultation.  Some  types  of  arrhythmias  are  also  recognized  by  inspec- 
tion at  the  apex.  The  regular,  slow  ventricular  activity  of  heart  block, 
the  irregular  ventricular  action  of  auricular  fibrillation,  the  apparent 
intermission  of  cardiac  activity  denoting  premature  contraction  —  all 
these  are  often  distinguishable  upon  inspection  of  the  apical  region.  The 
extrasystolic  contraction  itself  is  rarely  seen  because  it  is  usually  too 
weak  to  cause  a  visible  ventricular  impact.  The  movement  of  the 
apical  region  during  the  respiratory  phases  may  likewise  be  discernible 
in  thin  or  moderately  thick-chested  individuals  who  possess  a  fair  amount 
of  diaphragmatic  excursion. 

Inspection  of  the  Right  Lower  Interspaces.  —  Over  the  right  lower 
chest,  aside  from  aneurism  and  aneurismal  dilatations  already  mentioned, 
very  little  information  can  be  gleaned  by  inspection.  Right  auricular  and 
right  ventricular  enlargement  rarely  give  rise  to  visible  pulsation.  I  have 
met  with  isolated  exceptions,  however.  One  case  was  that  of  a  boy  of 
17  with  a  double  mitral  lesion  and  a  somewhat  enlarged  liver.  At  the 
time  of  hospital  admission  he  was  suffering  from  an  acute  rheumatic 
exacerbation  of  endocarditis.  To  the  right  of  the  sternum,  in  the 
third  and  fourth  interspaces,  there  was  a  visible  pulsatile  area  approxi- 
mately the  size  of  a  pigeon's  egg.  Over  this,  there  was  heard  a  very 
loud  harsh  murmur,  a  rough  palpable  thrill  was  present ;  both  were 
systolic  in  time.  Fluoroscopic  examination  showed  that  the  pulsation 
was  due  to  a  greatly  enlarged  right  auricle.  The  patient  died  a  few 
weeks  later.  At  necropsy,  a  double  mitral  lesion,  an  hypertrophied  right 
and  left  ventricle,  and  a  hugely  dilated,  engorged,  and  thickened  right 
auricle  were  found.  In  situ  in  the  chest  cavity,  the  longest  measure- 
ment of  the  auricle  was  17  cm.,  its  broadest  8  cm.  (Fig.  241).  In 
another  instance  of  decompensated  double  mitral  lesion  in  a  woman  of 
26,  intensely  dyspnoeic,  cyanotic,  and  with  a  pulsating  liver,  there  was 
a  similar  though  less  prominent  visible  auricular  pulsation  in  the  third 
and  fourth  right  interspaces  ;  a  thrill  was  also  heard  over  the  same  area. 

Visible  epigastric  pulsation  in  patients  with  dilated  and  hypertro- 
phied hearts  is  fairly  common.     It  is  usually  attributed  to  hyper- 


132 


CLINICAL  CARDIOLOGY 


trophic  enlargement  of  the  right  ventricle,  but  necropsy  reports  have 
not  always  substantiated  this  supposition  (Chapter  XV). 

Liver  pulsation  is  not  infrequent  in  decompensated  mitral  lesions, 
or  in  relative  tricuspid  regurgitation.  It  is  less  common  in  aortic  lesions. 
The  pulsations  may  be  sufficiently  gross  to  be  seen  at  a  distance;  at 
other  times,  close  examination,  especially  with  the  observer's  eye 
placed  on  a  level  with  the  patient's  abdomen,  is  necessary  in  order  to 
discern  the  pulsating  liver.     Auricular  fibrillation  may  occasionally  be 


A-- 


A- 


Fig.  241.  —  Outline  of  the  heart  in  situ  (reduced  X  5). 
A  =  dilated  right  auricle ;  B  =  midline  of  the  body ;  C  =  enlarged  right  ventricle. 


diagnosed  by  inspection  of  the  liver,  if  its  pulsations  are  manifestly 
and  grossly  arrhythmic. 

Palpation 

Palpation  in  the  neck  often  substantiates  the  information  gained 
by  inspection.  Extrasystoles  may  be  felt  in  the  carotids  when 
they  are  missed  at  the  wrist.  Overacting  hearts  (for  example, 
exophthalmic  goiter)  often  produce  palpable  systolic  carotid  thrills ; 
these  may  be  due  to  whorls  and  eddies  from  the  violence  with  which 
the  blood  is  thrown  into  the  arterial  circulation.  Such  short,  sharp 
thrills  must  be  distinguished  from  the  steadier  and  longer  continued 
ones    accompanying    rheumatic    aortic    stenosis   and   arteriosclerotic 


PHYSICAL  EXAMINATION   OF   THE   HEART         133 

roughening  and  thickening  of  the  aortic  valves  and  walls.  The  typical 
quick  filling  and  collapsing  pulse  of  aortic  regurgitation  can  also  be 
readily  diagnosed  by  palpation  alone.  A  point  insufficiently  emphasized 
is  the  knowledge  regarding  arteriosclerosis  which  may  be  gained  by 
carotid  palpation;  the  condition  of  the  external  carotids,  whether 
tortuous,  thick,  hard  and  non-elastic,  or  the  reverse,  is  thus  often  de- 
termined. Similar  information  is  occasionally  derived  by  palpation  of 
the  common  carotid. 

Palpation  of  the  Aorta.  —  With  a  normal  cardiovascular  system 
and  an  aortal  arch  situated  moderately  high  in  the  chest,  the  finger 
tip  placed  in  the  interclavicular  notch  and  insinuated  behind  the  manu- 
brium recognizes  aortal  pulsation  as  a  soft  quiet  impact.  In  marked 
hypertension  a  sense  of  sharp  fling  is  often  given  to  the  examining 
finger.  In  luetic  aortitis  with  aneurismal  dilatation,  there  is  a  feeling 
of  a  broad,  strong  aortic  impact,  especially  when  decompensation  is 
present ;  this  is  sometimes  combined  with  a  palpable  thrill.  The  rough 
thrill  accompanying  aortic  stenosis,  and  the  sharp  rise  and  subsequent 
collapse  of  the  aortal  walls  in  aortic  regurgitation,  can  also  be  diagnosed 
by  palpation  in  the  jugulum. 

Palpation  over  the  base  of  the  heart,  on  the  right  side,  may  be  of 
great  diagnostic  importance.  In  extreme  cases  of  rheumatic  aortic 
stenosis  a  rough  rasping  systolic  thrill  is  readily  felt  in  the  second  and 
third  right  interspaces.  The  overacting  aorta  in  aneurism  and  aneuris- 
mal dilatation  of  the  first  part  of  the  aorta,  and  the  sharp  aortic  disten- 
tion in  hypertension,  are  sometimes  palpable  over  the  same  area.  When 
present  in  the  former,  this  probably  denotes  an  extremely  roughened, 
thickened  aortal  wall,  or  extreme  dilatation.  Bulging  of  the  right 
anterior  chest,  found  in  adherent  or  erosive  aneurisms,  is  obviously 
palpable.  Aneurisms  or  aneurismal  dilatation  of  the  descending  part 
of  the  arch,  or  even  of  the  descending  thoracic  aorta,  may  occasionally 
be  felt  by  placing  the  fingers  snugly  against  the  chest  over  the  base  of 
the  heart,  on  the  left  side,  or  in  the  third  and  fourth  left  interspaces. 
In  the  latter  position,  the  location  of  the  impact  area  near  the  sternum, 
and  the  time  of  its  appearance,  serve  to  distinguish  it  from  the  impact 
due  to  ventricular  systole  (Chapter  XIV). 

In  congenital  pulmonary  stenosis  and  in  patent  ductus  arteriosis, 
thrills,  usually  systolic  in  time,  are  often  palpable  over  the  left  basal 
region.  In  congenital  patent  interventricular  septum,  there  is  a 
rough,  harsh  thrill,  systolic  in  time,  palpable  over  the  entire  precordium, 
but  especially  over  the  lower  sternum.  In  patients  with  dilated  and  over- 
acting pulmonary  arteries,  the  sharp  click-like  closure  of  the  valves 
can  occasionally  be  felt  by  palpation  over  their  site.  This  condition, 
combined  with  a  murmur  over  the  same  area,  is  common  in  the  mitral 
valvulitis  in  children,  in  whom  it  is  sometimes  incorrectly  diagnosed  as 
a  congenital  pulmonary  lesion.  Similar  hyperaction  is  occasionally 
present  as  a  temporary  phenomenon  in  normal  individuals. 


134  CLINICAL  CARDIOLOGY 

Palpation  in  Mitral  Lesions. — In  typical  mitral  stenosis,  with  the 
heart  beating  rhythmically,  there  is  a  short  presystolic  thrill  palpable  in 
the  apical  region.  When  the  auricles  fibrillate  and  the  ventricles  beat 
irregularly  and  tumultuously,  an  intense  and  rough  thrill,  most  promi- 
nent at  the  apex  and  occupying  a  varying  part  of  the  diastole,  may  be 
felt ;  if  the  irregular  ventricular  activity  be  controlled  by  digitalis,  the 
thrill  becomes  less  marked  or  entirely  disappears.  A  palpable  systolic 
thrill  over  the  lower  precordium  not  infrequently  accompanies  rheumatic 
regurgitant  lesions,  and  may  indeed  be  present  when  the  murmur  itself 
is  faint  or  absent.  This  condition  was  found,  for  example,  in  a  young 
girl  without  any  previous  rheumatic  history ;  she  had  had  frequent 
attacks  of  dyspnoea,  and  edema  of  the  face  and  extremities.  At  the 
apex  a  scarcely  perceptible  murmur  was  heard  ;  it  was  not  transmitted. 
Over  the  lower  precordium  there  was  a  very  pronounced  palpable  thrill. 
Systolic  precordial  thrills  may  also  be  felt  when  the  mitral  cusps  are 
thickened  or  covered  with  lime  deposits  as  the  result  of  a  cardiosclerotic, 
non-rheumatic  process  (Chapter  XII). 

Further  information  regarding  the  character  of  ventricular  contrac- 
tion and  of  the  apex  beat  can  be  gained  by  applying  the  flattened  palm 
snugly  over  the  lower  precordial  area.  The  booming  broad  ventricular 
shock  and  diffuse  apical  impact  of  hypertrophy  may  thus  be  readily 
diagnosed,  particularly  if  the  heart  action  is  of  normal  rapidity  or 
abnormally  slow.  Rapid  action,  even  of  a  normal  sized  heart,  usually 
gives  the  impression  of  enlargement,  probably  because  of  the  rather 
violent  impact  against  the  chest  wall.  I  have  often  corroborated  the 
normal  size  of  such  hearts  by  fluoroscopic  examinations.  A  somewhat 
thrill-like  sensation  is  imparted  to  the  examining  hand  during  systole  by 
violent  ventricular  overaction  which  usually  accompanies  tachycardia 
from  any  cause.  Here  the  thrill  may  be  due  to  sharp  vibratory  action 
of  the  auriculo-ventricular  valves  transmitted  through  the  chest  wall 
during  violent  ventricular  systole.  If  the  chest  wall  is  of  moderate  thick- 
ness, it  is  sometimes  possible  to  recognize  the  weakened  impulse  of  an  en- 
larged dilated  heart  by  palpation.  A  double  systolic  apical  impact,  cor- 
responding to  the  reduplicated  first  sound  (so-called  gallop  rhythm,  q.v.), 
may  also  be  distinguished  by  palpation  over  the  apex,  especially  when 
due  to  left  ventricular  hypertrophy,  hypertension,  or  to  aortic  valvular 
lesions.  The  etiology  of  these  reduplications  will  be  discussed  in  con- 
nection with  auscultation.  Finally,  pulsus  paradoxus  may  be  diagnosed 
by  palpation,  by  the  gradations  of  strength  of  ventricular  contractions 
corresponding  to  the  rhythmic  waning  and  waxing  of  the  pulse  volume 
with  inspiration  and  expiration.  This  is  commonly  attributed  to  peri- 
carditis with  effusion,  or  to  intrathoracic  tumors.  I  have  observed 
it  in  occasional  cases  of  myocarditis  with  severe  decompensation,  or 
in  the  agonal  stage  of  cardiac  failure. 


PHYSICAL  EXAMINATION   OF  THE   HEART  135 


Percussion 

To  the  ordinary  and  older  methods  of  ringer  and  pleximeter 
hammer  percussion  have  been  added  the  auscultatory,  and,  more 
recently,  the  flexed  finger  (Goldscheider's  orthopercussion)  methods. 

The  auscultatory  method  consists  in  placing  the  bell  of  the  stethoscope 
over  the  center  of  the  sternum  and  noting  when  scratch  marks  or  light 
tappings  made  by  the  finger  nail  or  finger  tips  first  become  audible. 
Orthopercussion  consists  in  light  perpendicular  tapping  over  a  sharply 
flexed  finger  held  perpendicularly  to  the  chest  wall  and  acting  as  the 
pleximeter.  These  two  methods  were  advanced  as  refinements  by  which 
the  exact  cardiac  border  could  be  more  delicately  and  accurately  out- 
lined. 

Inaccuracy  of  Percussion  Methods.  —  Careful  and  continued  use 
and  observation  of  the  above,  as  well  as  of  the  usual  methods,  checked 
by  comparison  with  the  unequivocal  standards  furnished  by  orthodias- 
copy and  fluoroscopy,  have  convinced  me  that  all  methods  of  percussion 
are  inaccurate  and  unreliable  even  for  clinical  purposes.  Besides 
varying  among  themselves  considerably  in  accuracy,  there  is  no  means  of 
judging  in  advance  which  method  will  prove  sufficiently  exact  in  any 
individual  case.  In  many  instances,  I  have  requested  experienced  and 
excellent  clinicians  to  map  out  the  cardiac  border  according  to  their 
own  favorite  method  of  percussion,  and  I  have  demonstrated  to  them  by 
fluoroscopy  that  the  results  of  their  examination  were  rarely  of  sufficient 
exactness  even  for  general  bedside  purposes.  These  statements  apply 
to  percussion  for  superficial  dullness  as  well  as  for  flatness.  For  example, 
very  marked  aortic  dilatations  were  at  times  entirely  overlooked ;  defi- 
nite extension  of  the  cardiac  border  to  the  right  was  not  even  approxi- 
mately delimited.  My  own  gross  errors  by  the  various  methods  of 
percussion  have  included  practically  all  miscalculations :  the  delimita- 
tion of  the  size  and  of  the  upper  border  of  the  aorta,  the  right  border 
of  the  heart,  and  the  upper  ventricular  border.  Figures  242  to  246 
demonstrate  some  of  these  errors  in  patients  with  normal  and  abnormal 
hearts,  in  whom  mistakes  of  outline  varying  from  several  centimeters 
to  almost  grotesque  proportions  have  been  committed.  From  the 
viewpoints  of  physics  and  acoustics,  there  seem  to  be  good  reasons  for 
diagnostic  errors  in  the  use  of  percussion.  Unless  greatly  enlarged  and 
near  the  surface,  the  aorta,  situated  as  it  normally  is  mainly  behind  the 
sternum,  is  scarcely  sufficiently  thick-walled  or  with  its  contained  blood 
of  a  sufficient  density  to  cause  differential  dullness  or  flatness  on  per- 
cussion. Similar  reasons  make  difficult  the  delimitation,  by  percus- 
sion, of  the  right  cardiac  border,  consisting  of  the  right  auricle  below 
and  the  great  vessels  above.  Percussion  of  the  left  ventricular  area  is 
surrounded  by  less  difficulties,  for  the  ventricular  mass  is  denser  and 
more  uniform ;  but  its  approximate  size  and  contour  —  whether  squatty, 
broad,  erect,  or  gracile,  subjects  already  discussed  in  connection  with 


136 


CLINICAL  CARDIOLOGY 


Fig.   242.  —  Normal  heart  —  thin-chested         Fig.    243.  —  Normal  heart  —  thick-chested 
male.  male. 


Fig.  244.  —  Normal  heart —  normal-chested  male. 


/ 


Fig.    245.  —  Mitral    stenosis    and    regurgita-        Fig.    246.  —  Aneurismal    dilatation    and 
tion  —  normal-chested  female.  left   ventricular    hypertrophy  —  thin- 

chested  male. 
Figs.  242-246.  —  Difference  in  percussion   (dotted   lines)  and  orthodiascopic  (solid  lines) 
outlines  of  normal  and  abnormal  hearts. 


PHYSICAL  EXAMINATION   OF  THE   HEART         137 

orthodiascopy  (Chapter  IX)  —  are  considerations  which  I  believe  are 
beyond  the  physical  limits  of  percussion.  Frequent  comparisons  be- 
tween percussion  and  radiographic  findings  have  also  convinced  me 
that  the  left  border  of  the  heart  may  actually  be  several  centimeters 
beyond  the  percussed  outline,  and  that  the  lower  point  of  the  heart  — 
the  apex  as  viewed  fluoroscopically  at  the  end  of  inspiration  —  is  usually 
from  2  to  5  cm.  below  its  position  as  located  by  percussion  or  palpa- 
tion. This  difference  between  the  '  palpable  '  and  '  fluoroscopic  '  apex 
is  especially  noticeable  in  tall,  lean  individuals  with  flat  chests,  narrow 
elongated  hearts,  and  mobile  diaphragms. 

A  Rational  Method  for  the  Determination  of  the  Cardiac  Outline.  — 
In  view  of  the  limitations  and  of  the  inaccuracy  of  the  percussion 
methods,  I  have  attempted  to  apply  the  more  exact  knowledge  gained 
by  roentgenography  to  bedside  study  of  the  cardiac  outline.  The  routine 
I  use  for  this  purpose  is  as  follows :  First,  inspection,  and  then  palpa- 
tion of  the  precordium.  Then  auscultation  to  determine  the  presence 
and  type  of  a  possible  cardiac  lesion.  Finally  the  mapping  out  of  the 
cardiac  outline.  The  initial  step  in  the  latter  procedure  consists  in  an 
attempt  to  determine  the  upper  aortal  border ;  this  is  accomplished  by 
insinuating  the  tip  of  the  finger  in  the  jugulum.  If  the  arch  of  the  aorta 
is  situated  high  in  the  thorax,  it  can  be  thus  palpated  ;  its  corresponding 
upper  limit  is  then  marked  on  the  chest  wall.  If  the  aorta  cannot  be 
palpated  in  this  manner,  it  is  considered  as  '  low.'  Its  approximate 
position  may  then  be  roughly  determined  by  noting  the  most  prominent 
point  at  which  the  aortic  sounds  are  heard  over  the  right  base.  This 
marks  the  probable  position  of  the  aortic  valves ;  the  upper  aortal 
border  lies  about  2  or  3  cm.  above  this  point.  The  next  fixed  point 
to  be  charted  on  the  chest  wall  is  that  of  the  maximal  apical  impulse. 
In  adults  this  is  best  determined  by  auscultation;  in  children,  by 
palpation.  As  already  stated,  the  actual  position  of  the  apex,  as  de- 
termined by  fluoroscopy  at  the  end  of  inspiration,  is  commonly  2  to  5 
cm.  below  the  point  of  maximal  apical  impulse;  it  varies  with  the 
amount  of  diaphragmatic  excursion  and  the  type  of  cardiac  contour 
(Chapter  IX).  In  most  cases,  these  two  variants  can  be  estimated 
with  some  accuracy,  even  at  the  bedside,  from  the  experience  and 
knowledge  gained  by  fluoroscopic  examinations.  Thus,  in  an  individual 
with  a  normal  heart,  one  variant  —  the  type  of  cardiac  contour  —  can 
often  be  roughly  foretold  by  the  configuration  of  the  chest  and  extrem- 
ities, and  by  the  type  of  general  physique.  If  an  individual  is  thick- 
set, with  short  and  pudgy  hands,  the  heart  is  apt  to  be  broad  and 
flat,  and  the  actual  position  of  the  apex  will  not  be  much  below 
the  point  of  maximal  apical  impulse.  The  lower  right  cardiac  border 
(the  right  auricular  border)  is  ordinarily  from  3  to  5  cm.  to  the  right 
of  the  midsternal  line.  If  the  individual  is  tall,  spare,  and  thin-chested, 
with  graceful  extremities,  the  cardiac  contour  is  usually  long  and  narrow, 
the  actual  apex  well  below  the  palpable  impulse,  and  the  right  auricular 


138  CLINICAL  CARDIOLOGY 

border  close  to  the  right  sternal  margin.  Exceptions  in  thin  individuals  ■ 
are  readily  noted  by  the  position  of  the  apex.  The  second  variant  — 
diaphragmatic  excursion  —  is  more  readily  estimated.  It  depends  upon 
lung  expansion  and  upon  the  amount  and  thickness  of  the  abdominal 
and  chest  walls.  In  obese  patients  with  thick  chest  walls,  diaphragmatic 
mobility  is  limited;  the  reverse  is  the  case  in  well-knit  persons  with 
good  lung  expansion.  Bearing  these  simple  facts  in  mind,  the  true 
position  of  the  apex  may  be  readily  and  fairly  accurately  gauged.  I  had 
attempted  to  outline  the  remainder  of  the  cardiac  contour — the  right 
aortal,  and  the  borders  of  the  pulmonary  artery  —  by  seeking  the  points 
over  the  right  and  left  bases  at  which  aortic  and  pulmonary  sounds 
are  heard  most  prominently.  However,  I  have  not  found  this  method 
more  accurate  than  merely  drawing  the  cardiac  outline  of  the  normal 
heart  by  using  the  landmarks  already  determined  —  the  upper  aortal 
border,  the  calculated  position  of  the  actual  apex,  the  right  border,  and 
the  presumed  type  of  cardiac  contour,  as  guides  for  completing  the  out- 
line. In  this  manner,  in  a  series  of  normal  hearts,  I  have  in  the  majority 
of  instances  been  able  to  gauge  the  cardiac  outline  with  sufficient  ac- 
curacy for  clinical  purposes,  and  have  at  any  rate  avoided  any  gross 
miscalculations,  as  shown  by  comparisons  with  the  fluoroscopic  ex- 
aminations. 

Determination  of  the  Cardiac  Outline  in  Cardiac  Disease.  —  In 
cardiac  disease,  in  addition  to  the  above  landmarks,  further  knowledge 
regarding  the  size  of  the  heart  is  gained  from  palpation  and  ausculta- 
tion; definite  inferences  may  thus  be  derived  regarding  the  probable 
shape  as  well  as  size  of  the  heart.  For  example,  in  hypertension  with 
an  enlarged  left  ventricle  and  a  booming  apex  beat,  the  lowermost  part  of 
the  heart  (the  '  fluoroscopic  apex ')  will  be  found  considerably  below  the 
point  of  maximal  apical  impulse,  and  the  cardiac  outline  will  thus  be 
found  very  much  enlarged  not  only  to  the  left  but  also  downwards. 
In  decompensated  mitral  lesions  with  diffuse  apical  impulse,  especially 
with  auricular  fibrillation,  the  right  auricular  border  will  be  considerably 
to  the  right  of  the  midsternal  line,  and  the  '  actual  apex  '  mainly  to  the 
left  and  not  much  below  the  usual  position  of  the  normal  apex. 

It  is  true  that  the  method  above  described  contains  various  in- 
accuracies, but  I  have  found  that  careful  balancing  of  the  factors  in- 
volved leads  to  closer  and  more  reliable  information  than  dependence 
upon  any  method  of  percussion.  Perhaps  further  studies  along  these 
lines  will  yield  more  accurate  data. 

Auscultation 

Despite  drawbacks  and  opportunities  for  error,  auscultation  is 
the  most  accurate  of  the  four  methods  for  the  detection  of  the  type  of 
valvular  or  myocardial  disease.  The  presence  of  cardiac  murmurs  (by 
which  are  meant  adventitious  sounds,  not  merely  modifications  of  the 


PHYSICAL  EXAMINATION   OF  THE  HEART         139 

normal),  their  time  relationship  to  events  in  the  cardiac  cycle,  their 
intensity,  quality,  pitch,  timbre,  and  the  direction  of  their  propa- 
gation over  the  precordium  as  well  as  through  the  larger  arteries, 
the  presence  of  audible  thrills  and  rumbles,  all  require  auscultation 
for  their  recognition.  It  is  important  to  remember  that  murmurs 
may  change  in  character  with  change  in  the  patient's  position."  They 
are  usually  more  intense  when  the  patient  is  lying  down;  this  may 
be  because  in  other  positions  (standing  or  sitting)  the  apical  impulse 
masks  the  murmur.  Rapid  heart  action  commonly  intensifies  the 
murmur  of  a  mitral  stenotic  lesion  although  its  duration  is  considerably 
diminished.  For  purposes  of  careful  auscultation,  one  may  attempt  to 
slow  the  cardiac  rate  by  having  the  patient  breathe  deeply  and  slowly ; 
and  to  accelerate  the  heart  action,  by  asking  the  patient  to  take  a 
few  rapid  breaths.  Another  consideration  which  occasionally  modifies 
both  normal  sounds  and  murmurs  is  the  amount  of  pressure  used  when 
applying  the  stethoscope  to  the  chest  wall. 

Valvular  Murmurs  in  Rheumatic  Endocarditis. — Organic  valvular 
defects  do  not  always  produce  murmurs.  It  is  sometimes  difficult 
from  auscultation  alone  to  determine  which  valve  is  affected,  or  to  dis- 
tinguish valvular  from  non-valvular  affections.  Other  differential 
criteria  will  be  discussed  later.  As  further  complicating  factors  in 
auscultation,  the  intensity  and  the  propagation  of  the  murmurs  are 
considerably  modified  by  the  state  of  cardiac  compensation,  the  amount 
of  dilatation  and  hypertrophy,  the  rapidity  of  heart  action,  and  the 
thickness  of  the  chest  wall. 

Organic  valvular  murmurs  are  best  grouped  into  those  due  to 
narrowing  of  the  caliber  of  the  valvular  orifice  (stenotic  lesions)  and 
those  allowing  leakage  (regurgitant  lesions). 

A  mitral  regurgitant  lesion  produces  a  murmur  systolic  in  time ; 
the  second  pulmonic  sound  is  often  accentuated.  The  murmur  may  be 
soft  and  blowing  in  character,  occupying  only  a  part  of  the  systole, 
and  accompanying,  not  replacing,  the  first  sound.  When  typical  and 
well  marked,  the  murmur  is  rough,  low  pitched,  occupies  the  entire 
systole,  replaces  the  first  sound,  is  heard  loudest  in  the  apical  region, 
and  is  transmitted  laterally  to  the  axilla.  More  rarely  it  is  heard  over 
the  entire  precordium.  It  is  sometimes  heard  posteriorly  between  the 
angle  of  the  left  scapula  and  the  spinal  column,  especially  in  children. 
The  murmur  may  be  accompanied  by  a  palpable  thrill.  In  decom- 
pensation with  cyanosis  a  diastolic  murmur  transmitted  downwards 
(the  Graham-Steele)  is  occasionally  heard  at  the  second  right  inter- 
space; it  is  probably  due  to  dilatation  of  the  pulmonary  orifice  with 
consequent  relative  insufficiency. 

Mitral  Stenosis.  —  In  this  lesion  the  second  pulmonic  is  frequently 
accentuated  as  compared  with  the  second  aortic  sound.  The  murmur 
itself  is  caused  by  auricular  contraction  forcing  blood  through  a  narrowed 
mitral  orifice;   the  name  auriculo-systolic  given  to  this  murmur  many 


140  CLINICAL  CARDIOLOGY 

years  ago  by  Gairdner  aptly  describes  its  mechanism.  It  is  character- 
istically a  rough,  rasping  vibrant  murmur ;  there  is  often  a  reduplicated 
second  sound  at  the  apex.  The  murmur  seems  crescendo  in  character,  but 
electrocardiographic  sound  records  tend  to  show  that  this  'crescendo' 
quality  is  only  produced  by  its  proximity  to  the  loud  first  sound.  The 
time  of  appearance  of  the  murmur  is  immediately  preceding  systole 
(presystolic)  or  in  late  diastole.  It*  may  occupy  the  entire  diastole. 
It  is  occasionally  mid-diastolic,  with  a  distinct  gap  between  its  com- 
pletion and  the  following  systole.  This  has  been  demonstrated  by 
electrocardiographic  sound  records  from  patients  in  whom  there  was 
prolonged  auriculo-ventricular  conduction  time  (usually  caused  by 
digitalis) ;  the  murmur  always  occurred  at  the  time  of  auricular  systole, 
which  in  these  cases  bore  varying  relations  to  the  diastole.  A  similar 
instance  came  under  my  observation  —  a  young  woman  with  mitral 
stenosis  and  gastric  symptoms.  Electrocardiographic  tracings  showed 
progressively  prolonged  P-R  intervals  (Chapter  VII),  so  that  at  times 
there  were  independent  auricular  contractions;  the  rough,  rasping 
murmur  was  always  synchronous  with  auricular  systoles,  and,  depending 
upon  the  conduction  time,  was  heard  in  varying  places  in  diastole. 
Such  observations  clinch  the  cause  of  the  mitral  stenotic  murmur  as 
due  to  auricular  contractions.  The  mitral  stenotic  murmur  often 
varies  in  intensity  and  duration.  These  variations  probably  depend 
upon  the  rate  with  which  the  blood  flows  from  auricle  to  ventricle 
(Lewis),  which  in  turn  depends  upon  the  difference  in  pressure  existing 
in  these  two  chambers.  In  the  normal  heart,  at  the  beginning  of  ven- 
tricular diastole  (and  therefore  of  ventricular  filling),  the  auricular 
pressure  is  high,  the  rate  of  flow  more  rapid.  With  the  filling  of  the 
ventricle,  the  difference  between  ventricular  and  auricular  pressure 
becomes  less  and  less  until  the  advent  of  auricular,  which  of  course 
immediately  precedes  ventricular  systole.  At  this  time  there  is  a  sharp 
rise  of  auricular  pressure  and  an  increased  rate  of  flow  into  the  ventricle. 
Applying  these  facts  to  the  slow,  rhythmically  beating  heart  with  mod- 
erate mitral  stenosis,  the  differential  auriculo-ventricular  pressure  is 
manifest  only  at  auricular  systole,  consequently  the  murmur  with  this 
type  of  rhythm  is  presystolic  only.  With  more  marked  stenosis,  or 
with  more  rapid  heart  action  (shortened  diastole),  the  differential  pres- 
sure favors  the  auricle  at  the  immediate  completion  of  the  ventricular 
systole;  hence,  here  the  murmur  occurs  not  only  in  presystole  but 
also  in  early  diastole,  or  may  occupy  the  entire  diastolic  period.  It  is 
especially  in  auricular  fibrillation  that  the  murmurs  of  mitral  stenosis 
undergo  marked  changes.  Absence  of  rhythmic  auricular  contraction 
precludes  the  usual  presystolic  element  of  the  diastolic  murmur.  With 
comparatively  slow  and  regular  ventricular  action,  there  is  a  distinct 
pause  between  the  diastolic  murmur  and  the  following  systole.  The 
murmur  may  occupy  early  diastole  alone  and  gradually  wane  because 
the  auricular  is  then  greater  than  the  ventricular  pressure  and  diminishes 


PHYSICAL  EXAMINATION   OF   THE   HEART         141 

with  the  filling  of  the  ventricle.  A  rough,  rasping  diastolic  murmur 
and  a  palpable  thrill  may  lose  these  characteristics  under  the  influence 
of  digitalis  and  become  much  softer  and  scarcely  audible.  I  believe 
this  is  because  digitalis  has  produced  steadier  ventricular  contraction 
with  lessened  differences  in  auriculo-ventricular  pressure  following 
ventricular  systoles.  When  the  ventricle  beats  very  irregularly  and 
rapidly,  the  murmur  is  short,  sharp,  and  seemingly  occupies  the  entire 
shortened  diastolic  period.  With  extremely  rapid  and  tumultuous 
cardiac  activity  it  may  become  barely  audible  or  distinguishable, 
although  in  the  occasional  longer  diastolic  pauses  its  usual  character- 
istics are  evident. 

Aortic  Stenosis.  —  When  typical,  the  murmur  accompanying  ex- 
treme aortic  stenosis  is  the  most  marked  of  all  the  valvular  lesions. 
It  is  then  loud,  rough,  and  vibrant,  is  systolic  in  time,  is  heard  best 
in  the  second  right  interspace  and  is  transmitted  along  the  carotids. 
It  is  occasionally  transmitted  downward  or  posteriorly  at  the  level 
of  the  third  or  fourth  dorsal  vertebra.  The  second  aortic  sound  is 
often  absent.  This  rough  murmur  is  accompanied  by  a  systolic  thrill 
felt  over  the  right  base  and  carotids.  The  pulse  wave  may  rise  slowly 
(pulsus  tardus,  Chapter  III),  a  characteristic  sometimes  recognizable 
by  radial  palpation. 

Aortic  Regurgitation.  —  This  murmur  varies  considerably  in  intensity 
and  in  propagation.  It  is  diastolic  in  time  and  may  occupy  only  the 
beginning  or  the  entire  diastole.  It  usually  replaces  the  second  sound. 
The  murmur  is  most  often  blowing  in  character ;  may  be  very  soft,  or, 
occasionally,  quite  loud  and  rough.  The  usual  area  of  greatest  intensity 
is  at  the  right  base ;  however,  it  is  often  heard  loudest  at  the  second 
and  third  left  interspaces  near  the  sternum.  Not  infrequently  an 
aortic  regurgitant  murmur  has  exactly  the  characteristics  of  a  mitral 
stenotic  one ;  that  is,  it  produces  a  presystolic  sharp  rumble  at 
the  apex  (Austin  Flint  murmur).  Under  such  circumstances,  the 
regurgitant  murmur  at  the  base  may  be  faint  or  entirely  absent.  Many 
theories  have  been  advanced  for  the  presence  of  this  presystolic  apical 
murmur  of  aortic  regurgitation,  but  as  yet  no  satisfactory  explanation 
has  been  given.  The  consensus  of  opinion  is  that  it  is  due  to  narrowing 
of  the  mitral  orifice  from  the  regurgitant  stream  of  blood  in  the  ven- 
tricle. 

Tricuspid  valvular  lesions  are  very  infrequently  encountered.  The 
etiology  is  rarely  rheumatic,  more  often  it  is  of  streptococcic  or  luetic 
origin.  Of  the  two  types,  regurgitant  and  stenotic,  the  former  is  the 
more  common.  The  regurgitant  lesion  is  characterized  by  a  blowing 
systolic  murmur,  heard  best  at  the  lower  sternum,  and  transmitted  to 
the  right ;  it  is  often  accompanied  by  a  pulsating  liver  and  marked 
jugular  pulsation.  In  one  case  that  I  observed,  a  distinct  palpable 
thrill  was  also  present.  Tricuspid  stenosis  is  exceedingly  rare  and  has 
never  been  found  as  an  isolated  valvular  lesion;    it  has  been  very  in- 


142  CLINICAL  CARDIOLOGY 

frequently  diagnosed  during  life.  The  characteristic  murmur  is  de- 
scribed as  a  presystolic  rumble  most  prominent  in  midsternum  or  over 
the  xiphoid.  The  lesion  may  be  suspected  in  the  presence  of  extreme 
cyanosis,  right  auricular  hypertrophy,  and  marked  pulsation  in  the 
veins  of  the  neck  and  in  the  liver. 

Valvular  pulmonary  insufficiency  is  exceedingly  rare;  it  has  never 
been  observed  as  an  isolated  lesion  and  has  been  correctly  diagnosed 
in  only  a  very  few  instances.  The  murmur  is  described  as  blowing 
in  character,  diastolic  in  rhythm,  heard  best  over  the  left  second  and 
third  interspaces,  and  transmitted  downward.  It  is  usually  accom- 
panied by  other  endocardial  murmurs. 

Pulmonary  stenosis  commonly  occurs  as  a  congenital  lesion.  Its 
differentiation  from  aortic  stenosis,  which  sometimes  presents  similar 
auscultatory  signs,  may  be  made  from  the  fact  that  the  murmur  of  the 
latter  is  propagated  along  the  carotids,  while  the  pulmonary  stenotic 
murmur  is  transmitted  downward. 

A  combination  of  lesions  of  the  various  valves,  especially  the  aortic 
and  mitral,  is  very  common.  The  lesions  in  themselves  tend  to  cause 
inorganic  or  so-called  functional  murmurs  (q.v.)  from  the  various  degrees 
of  valvular  and  ventricular  dilatation  they  produce.  In  addition  the 
valvular  murmurs  may  not  be  typical ;  therefore  it  is  sometimes  diffi- 
cult or  even  impossible  to  determine  the  exact  valvular  lesions  that  are 
present.  The  problem  is  further  complicated  by  the  frequent  coexist- 
ence of  pericarditis  with  its  adventitious  sounds.  An  extremely  valu- 
able guide  in  the  differentiation  of  such  complicated  murmurs  is  careful 
comparative  auscultation  of  the  differing  quality,  pitch,  and  propaga- 
tion of  the  murmurs.  In  this  manner,  the  characteristic  murmur  of 
one  of  the  valvular  defects  may  be  followed  through  an  apparent  maze 
produced  by  the  presence  of  other  valvular  murmurs.  Furthermore 
much  information  is  gained  by  precordial  palpation,  which,  with  auscul- 
tation, may  act  as  a  guide  in  the  determination  of  enlargements  typical 
of  the  various  valvular  lesions. 

Murmurs  in  Atherosclerosis 

Besides  rheumatic  valvular  affections,  atheromatous  changes  in 
the  mural  endocardium,  in  the  mitral  valves,  and  in  the  aortic  valves 
and  walls  frequently  give  rise  to  murmurs.  The  presence  and  signifi- 
cance of  the  murmurs  due  to  such  changes  have  not  been  sufficiently 
emphasized.  Intraventricular  murmurs,  non-rheumatic  in  origin,  are 
often  present  in  cardiosclerosis.  The  cardiosclerotic  process  prevents 
coaptation  of  the  mitral  cusps  and  thus  produces  mitral  regurgitation. 
This  murmur  is  systolic  in  time  and  is  heard  best  over  the  lower  pre- 
cordium;  it  is  usually  less  loud  than  the  rheumatic  valvular  mitral 
regurgitant  murmur  and  is  transmitted  over  a  smaller  area.     Thicken- 


PHYSICAL  EXAMINATION   OF  THE   HEART         143 

ing  and  dilatation  of  the  aortal  walls,  common  in  aortitis,  give  rise  to  a 
loud  rough  systolic  murmur  over  the  right  base.  As  distinguished 
from  aortic  stenosis  the  murmur  is  less  rough  and  vibrant,  and  only 
rarely  propagated  along  the  carotids.  If  aortic  dilatation  is  marked, 
the  systolic  may  be  followed  by  a  short  diastolic  murmur,  due  to  re- 
gurgitation in  the  enlarged  aortic  cavity  or  to  valvular  insufficiency. 

Intracardiac  Murmurs  of  Non-organic  Origin 

Murmurs  arising  in  the  heart  and  not  due  to  organic  disease  have 
received  many  names  and  have  been  ascribed  to  various  causes.  They 
have  been  termed  accidental  murmurs,  hemic  murmurs,  adventitious 
sounds,  and  functional  murmurs.  They  have  been  ascribed  to  anemia, 
to  relative  valvular  insufficiency  allowing  leakage  and  regurgitation 
of  blood,  to  return  of  the  blood  in  the  large  venous  trunks.  It  is  ap- 
parent that  much  confusion  exists  regarding  both  the  terminology  and 
the  etiology  of  these  intracardiac  murmurs.  In  the  description  to  be 
given,  I  shall  apply  the  term  '  functional  murmur  '  to  those  adventitious 
cardiac  sounds  not  produced  by  an  organic  lesion. 

Functional  murmurs  are  very  common.  The  fact  that  they  can 
occur  without  cardiac  disease  and  without  producing  symptoms 
requires  emphasis.  They  are  often  merely  accidental  discoveries 
in  the  routine  physical  examination.  The  presence  of  these  murmurs 
in  the  healthy,  as  well  as  in  such  conditions  as  fever  and  anemia,  sug- 
gests a  varying  etiology.  The  chief  characteristics  of  the  non-organic 
murmur  are  its  softness  and  its  limitations  to  small  areas.  There  are 
numerous  exceptions,  however.  The  murmur  may  be  rather  loud, 
somewhat  rough,  and  when  found  in  the  lower  precordium,  may  be 
slightly  transmitted  above,  or  to  the  left.  These  exceptions  are  es- 
pecially frequent  in  children  and  young  adults.  The  most  common 
site  of  the  functional  murmur  is  at  the  apex.  It  is  systolic  in  time  and 
accompanies  the  first  sound,  usually  as  a  soft  whiff.  In  addition  to 
normal  individuals,  such  functional  murmurs  are  found  in  patients 
with  rapid  heart  action,  in  those  with  flabby  general  musculature, 
and  in  those  with  anemia.  In  anemic  individuals,  the  changed  charac- 
ter of  the  blood  is  usually  assumed  as  the  etiological  factor.  This 
hypothesis,  howTever,  is  not  based  upon  any  experimental  data.  In 
those  with  flabby  musculature,  I  believe  the  cause  to  lie  in  dilatation  of 
the  musculature  supporting  the  mitral  ring,  with  consequent  leakage 
and  regurgitation ;  this  is  commonly  termed  relative  insufficiency  of 
the  mitral  valves.  Perhaps  many  of  the  murmurs  in  the  anemic  (so- 
called  hemic  murmurs)  heard  in  this  location  have  the  same  etiology, 
for  grave  anemia  conduces  to  a  lack  of  proper  muscular  tone.  In 
tachycardia,  improper  and  faulty  closure  of  the  mitral  cusps,  alone  or 
in  addition  to  relative  mitral  insufficiency,  may  be  the  cause  of  the 
functional  murmur  at  the  apex. 


144  CLINICAL  CARDIOLOGY 

A  source  of  diagnostic  confusion  sometimes  exists  in  differentiating 
the  non-organic  intracardiac  murmur  heard  over  the  apex  from  the 
organic  murmur  of  mitral  insufficiency.  The  distinction  between 
typical  non-organic  and  typical  organic  mitral  regurgitant  murmurs  is 
not  difficult ;  the  latter  are  rougher,  louder,  and  are  heard  over  larger 
areas  than  the  former.  The  second  pulmonic  sound  is  apt  to  be  ac- 
centuated as  compared  with  the  second  aortic.  When  the  character- 
istics of  the  two  overlap,  as,  for  example,  in  rheumatic  fever  in 
which  the  fever  itself  or  the  endocarditis  may  cause  the  murmur, 
the  distinction  between  the  organic  and  functional  becomes  ex- 
ceedingly difficult.  In  doubtful  cases  with  fever,  examination  must 
be  made  after  the  fever  has  run  its  course  in  order  to  arrive  at 
definite  conclusions.  In  anemia,  the  association  with  other  '  hemic ' 
murmurs,  especially  systolic  murmurs  at  the  right  base,  aids  in  the 
differentiation.  The  correlation  of  other  data  —  lack  of  symp- 
toms of  heart  disease,  general  type  of  muscular  development,  occupa- 
tion (sedentary  or  otherwise),  the  type  of  heart  as  seen  fluoroscopically 
—  all  these  are  elements  which  require  consideration  in  the  differential 
diagnosis  between  functional  and  organic  murmurs.  Non-organic  mur- 
murs are  commonly  met  with  in  patients  of  sedentary  habits,  with  flabby 
general  musculature  and  ptosed  abdominal  organs.  The  distinction  in 
the  middle  aged  and  elderly  between  a  mitral  non-organic  murmur  and 
that  found  associated  with  myocarditis  is  of  extreme  importance.  The 
differentiation  must  be  based  upon  the  usual  characteristics  of  the  non- 
organic murmur.  If  it  is  soft,  blowing,  and  not  transmitted,  one  may 
infer  that  the  mitral  ring  is  dilated  and  that  the  murmur  is  of  func- 
tional origin.  The  diagnosis  of  myocarditis  must  then  be  predicated 
upon  the  usual  evidence  of  myocardial  insufficiency,  and  upon  the 
presence  of  an  intraventricular  murmur  (q.v.)  characteristic  of  athero- 
sclerosis. 

Aberrant  fibers  coursing  through  the  ventricle,  formerly  termed 
aberrant  tendons,  can  presumably  give  rise  to  loud  systolic  murmurs 
over  the  precordium.  There  seems  to  be  no  method  of  distinguishing 
these  from  other  non-organic  or  organic  murmurs.  The  tricuspid 
murmur  of  relative  insufficiency  may  occur  with  decompensation  from 
any  cause  of  venous  congestion  :  emphysema,  myocarditis,  endocarditis, 
etc.  A  systolic  murmur  of  varying  intensity  is  then  heard  over  the 
lower  sternum,  usually  transmitted  to  the  right ;  an  enlarged  pulsating 
liver  is  occasionally  present.  Sometimes  the  liver  pulsates  in  the  absence 
of  a  tricuspid  murmur.  Since  this  could  scarcely  occur  without  re- 
gurgitation, it  is  clear  that  the  latter  may  be  present  without  producing 
a  murmur.  The  frequency  of  relative  tricuspid  insufficiency  without 
valvular  disease  is  added  evidence  that  mitral  regurgitation  with  its 
murmurs  may  also  be  due  to  relative  valvular  insufficiency  and  to 
abnormal  dilatation  of  the  mitral  ring.  If  tricuspid  regurgitation  and 
cardiac  decompensation  are  extreme,  the  systolic  murmur  is  occasion- 


PHYSICAL  EXAMINATION   OF  THE   HEART         145 

ally  transmitted  posteriorly  on  the  right  side  between  the  mid-dorsal 
spine  and  the  angle  of  the  scapula. 

A  non-organic,  soft,  blowing  systolic  murmur  is  frequently  heard 
over  the  aorta,  particularly  in  anemia.  It  has  none  of  the  character- 
istics of  aortic  stenosis.  This  murmur  is  also  found  in  decompensated 
mitral  lesions.  Its  cause  is  not  known.  A  short  diastolic  aortic  mur- 
mur may  be  present  in  mitral  lesions,  possibly  due  to  relative  insuffi- 
ciency from  abnormal  dilatation  of  the  aortic  ring. 

Third  Heart  Sound.  —  In  a  large  proportion  of  young  normal  adults, 
a  faint  third  heart  sound  at  the  apex  in  mid-diastole  may  be  heard  by 
placing  the  patient  in  the  left  lateral  position.  It  is  soft  and  low  pitched. 
Phonocardiograms  of  the  sound  have  been  obtained.  The  explanation 
given  for  the  third  heart  sound  is  that  it  is  due  to  the  sudden  floating 
up  and  tension  of  the  auriculo-ventricular  valves  from  the  first  onrush  of 
blood  from  the  auricle  to  the  ventricle. 

Extracardiac  Non-organic  Murmurs.  —  Pericarditis  is  naturally  not 
included.  Of  non-organic  murmurs  of  extracardiac  origin,  the  most 
common  is  that  termed  the  cardiorespiratory  or  cardio-pulmonary.  It 
is  usually  soft  and  blowing  in  character,  systolic  in  time,  and  heard  best 
over  the  left  base.  Ocassionally  these  characteristics  change.  The  mur- 
mur can  be  rough  and  loud,  and  be  transmitted  along  the  left  sternal 
border  and  lower  precordium  as  a  somewhat  superficial,  squeaky  sound 
resembling  a  friction  sound.  The  cardio-respiratory  murmur  is  ascribed 
to  compression  of  lung  tissue  between  the  heart  and  chest  wall.  During 
inspiration,  the  lung  covers  a  large  part  of  the  root  of  the  pulmonary 
artery  and  the  upper  precordial  surface,  facts  which  can  readily  be 
corroborated  by  fluoroscopic  examination.  This  also  explains  why  the 
murmur  is  usually  heard  best  when  the  lung  becomes  inflated  at  the  end 
of  inspiration.  However,  it  is  sometimes  best  heard  at  the  end  of  ex- 
piration, possibly  because  in  some  patients  the  pad  of  lung  between  the 
chest  wall  and  the  heart  is  abnormally  large,  thus  diminishing  the 
transmission  of  the  murmur.  The  murmur  is  found  frequently  in 
children.  It  is  not  uncommon  in  frail  women  with  thin  chest  walls. 
The  fact  that  the  intensity  of  the  murmur  depends  upon  respiratory 
phases  and  that  it  is  never  accompanied  by  a  palpable  thrill  aids  in 
distinguishing  it  from  other  types  of  organic  cardiac  murmurs  heard 
in  this  area. 

Reduplicated  Sounds  and  Reduplicated  Apical  Impulses.  —  These 
reduplications  have  received  various  names,  the  most  common  being 
split  sounds,  gallop,  canter,  double,  and  triple  rhythm,  and  "  bruit  de 
rappel."  The  term  '  reduplication '  seems  preferable  because,  though 
many  of  its  etiological  factors  are  still  obscure  and  problematical,  it 
conveys  some  concrete  idea  of  the  underlying  phenomenon. 

Reduplicated  Second  Sounds  are  of  valvular  origin  and  can  usually 
be  clearly  defined  by  auscultation.  In  the  order  of  their  frequency,  re- 
duplicated second  sounds  are  heard  at  the  apex  alone,  at  the  apex  and 


146  CLINICAL  CARDIOLOGY 

right  base,  at  the  right  base  alone,  and  lastly  over  the  pulmonary  artery. 
The  time  of  their  occurrence  in  the  cardiac  cycle  and  the  study  of 
electrocardiographic  sound  records  demonstrate  that  they  are  due  to 
closure  of  the  semilunar  valves.  Their  presence  in  various  positions 
and  combinations  suggests  differing  etiology.  In  many  instances 
conclusions  regarding  the  cause  can  for  the  present  be  only  tentative. 
One  cause  of  reduplicated  second  sounds  is  asynchronous  closure  of  the 
pulmonic  and  aortic  valves.  In  this  type  the  elements  constituting 
the  reduplication  are  heard  very  close  to  each  other.  In  other  types,  the 
sound  elements  may  be  separated  by  a  distinct  hiatus.  In  these,  the 
first  part  is  undoubtedly  due  to  closure  of  the  semilunar  valves,  since 
it  occurs  in  the  cardiac  cycle  in  early  diastole  soon  after  the  A-V  valves 
open.  The  second  part  of  the  reduplication  has  been  ascribed  to  a  pro- 
cess somewhat  similar  to  the  causation  of  the  third  heart  sound,  that  is, 
to  quick  ventricular  filling  and  resulting  vibration  of  the  floating  cusps. 
This  explanation,  however,  appears  untenable,  for  the  reduplicated 
elements  seem  identical  on  auscultation  and  have  been  so  proven  by 
graphic  sound  records.  As  a  more  plausible  explanation,  it  appears  to 
me  that  a  sharp  systolic  wave  can  produce  a  secondary  reflux  wave 
which,  impinging  upon  the  already  closed  and  tense  semilunar  valves, 
sets  these  in  vibration  and  thus  causes  the  second  element  of  the  redu- 
plication. This  would  account  for  its  frequent  presence  in  tachycardia, 
in  mitral  stenosis,  and  over  the  great  vessels  at  the  base  of  the  heart. 

Reduplicated  first  sounds  are  usually  classified  under  "presystolic 
gallop  rhythm."  I  here  include  only  reduplicated  first  sounds  without 
reduplicated  apical  impulses,  from  which  I  believe  they  are  etiologically 
distinct.  Thus  limited,  reduplicated  first  sounds  (without  reduplicated 
apical  impulses)  are  heard  only  in  the  apical  region.  It  can  be  dem- 
onstrated by  simultaneous  electrocardiographic  sound  records  and 
electrocardiograms  that  the  first  element  of  this  type  actually  lies  in 
presystole,  and  hence  must  be  due  to  some  presystolic  event  in  the 
cardiac  cycle.  Most  probably  this  is  auricular  contraction.  The  oc- 
currence of  the  reduplication  may  depend  upon  a  hypertrophied  or 
overacting  auricle. 

Reduplicated  Apical  Impulse.  — This  type,  always  accompanied  by 
a  reduplicated  first  sound  but  of  different  origin  from  the  above,  is  found 
especially  in  conjunction  with  hypertrophied  left  ventricle  and  in 
aortic  disease.  It  is  occasionally  found  in  the  overacting  normal  heart. 
Upon  auscultation,  besides  the  double  first  sound,  there  is  a  distinct 
sense  of  a  double  shock  or  impulse,  often  evident  upon  palpation  alone. 
Since  the  reduplicated  apical  impulse  has  been  found  in  lesions  of  the 
main  branch  of  the  auriculo-ventricular  bundle,  ventricular  asyn- 
chronism  is  evidently  one  of  its  causes.  The  clinical  diagnosis  is  aided 
by  the  fact  that  bundle  lesions  are  usually  accompanied  by  signs  of 
myocarditis  and  by  regular  slow  pulse  rates  between  50  and  60  per 
minute. 


PHYSICAL  EXAMINATION   OF  THE  HEART         147 

In  addition  to  patients  with  bundle  lesions,  I  have  observed  identical 
double  apical  impulses  in  those  without  electrocardiographic  or  other 
indication  of  bundle  lesion.  In  several  such  instances  there  was  definite 
fluoroscopic  evidence  that  the  double  impact  was  due  to  a  secondary 
ventricular  movement  following  the  primary  systole.  The  exact  cause 
of  this  double  impact  I  could  not  definitely  determine.  In  an  effort  to 
seek  its  explanation,  the  following  must  be  recalled.  It  is  known  that 
the  normal  first  sound  is  composed  of  three  elements :  first,  tension  of 
the  auriculo-ventricular  valves ;  secondly,  the  muscular  element, 
ventricular  contraction;  and  thirdly,  ventricular  impact  against  the 
chest  wall.  The  first  element  of  the  reduplicated  sound  under  discus- 
sion is  probably  due  to  the  usual  three  normal  factors  above  enumerated. 
Regarding  the  second  part  of  the  reduplication,  it  is  difficult  to  state  to 
what  extent  and  proportion  these  three  factors  are  concerned.  To  re- 
turn to  the  fluoroscopic  examination  of  patients  with  this  reduplication, 
one  may  observe  not  only  the  ventricular  systole,  but  what  may  be 
termed  '  ventricular  fling,'  seemingly  comprising  different  areas ;  some- 
times this  involves  the  apex  alone,  at  others,  the  entire  left  ventricle 
seems  to  take  part  in  the  secondary  movement.  It  is  impossible  to 
determine  how  far  such  ventricular  fling  resembles  normal  physiological 
systolic  contraction.  It  may  represent  an  attempt  to  regain  ventricular 
tone  which  is  interfered  with  by  the  distention  produced  by  varying 
amounts  of  residual  blood  following  systole.  In  general,  it  seems  in 
harmony  with  clinical  observations  to  seek  mechanical  intraventricular 
causes  for  the  reduplicated  apical  impulse.  A  weakened  myocardium 
may  fail  to  properly  empty  the  overdistended  ventricle,  a  condition 
favorable  to  the  production  of  a  double  impulse  and  reduplicated  first 
sound.  A  similar  condition  can  occur  in  patients  with  long-continued 
fever ;  as  in  typhoid,  where  myocardial  weakness  may  be  only  tem- 
porary and  functional.  Again,  it  can  occur  in  those  suffering  from 
myocarditis  and  resultant  myocardial  insufficiency.  This  was  well 
illustrated  in  an  instance  of  alcoholic  myocarditis  in  which  at  necropsy 
the  ventricles  were  found  hypertrophied  and  riddled  with  scar  tissue. 
A  reduplicated  apical  impulse  was  present  during  the  stage  of  decom- 
pensation alone ;  the  electrocardiogram  showed  a  deep  M  complex 
(Chapter  IV).  When  compensation  was  temporarily  restored,  the 
double  apical  impulse  and  M  complex  disappeared,  the  ventricular 
complex  assumed  a  normal  outline. 

Reduplicated  apical  impulses  are  frequently  present  in  aortic  re- 
gurgitation. In  these  cases  they  may  be  directly  due  to  the  blood 
which  regurgitates  into  the  ventricle ;  this  then  produces  a  sharp  ventric- 
ular shock  which  becomes  audible  as  well  as  palpable  at  the  apex. 
A  double  apical  impulse  is  also  found  in  left  ventricular  hypertrophy 
with  hypertension.  The  violence  of  ventricular  action  and  the  impact 
of  residual  blood  may  here  account  for  the  second  element  of  the  re- 
duplication. 


148  CLINICAL  CARDIOLOGY 

REFERENCES 
Chapter  X 

Bard,  L. :  Du  Bruit  de  Galop,  etc. ;  Semaine  Medieale,  1906,  XXVI,  229. 
Bard,  L. :  De  la  Multiplication  anormale  des  Bruits  de  Cceur ;  Semaine  Medieale, 

1908,  XXVIII,  3. 
Flint's  Physical  Diagnosis  (Emerson). 
Gairdner,  W.  T. :   A  Short  Account  of  Cardiac  Murmurs ;   Edinburgh  Medical 

Journal,  1861-2,  VII,  438. 
Lewis,  T. :  Lectures  on  the  Heart. 
Lewis,  T. :    Observations  upon  Ventricular  Hypertrophy,  etc. ;  Heart,  1913-14, 

V,  367. 
Mackenzie,  J. :  Diseases  of  the  Heart. 

Nothnagel's  Encyclopedia — •  Diseases  of  the  Heart ;  American  Edition. 
Pawinski,  J. :    Die  Entstehung  und  klinische  Bedeutung  des  Galopprhythmus ; 

Zeitschrift  f.  klinische  Medizin,  1907,  LXIV,  70. 
Robinson,  G.  C. :    Gallop  Rhythm ;    American   Journal  of  Medical  Sciences, 

1908,  CXXXV,  607. 
Shattuck,  G.  C. :     Relation  of  Dullness  to  Cardiac  Outline ;    Boston  Medical 

and  Surgical  Journal,  1916,  CLXXIV,  30. 
Thayer,  W.  S. :   Further  Observations  on  the  Third  Heart  Sound ;  Archives  of 

Internal  Medicine,  1909,  IV,  297. 


CHAPTER  XI 

ETIOLOGY    OF   ENDOCARDITIS    AND    OF    CARDIOVASCULAR 

DISEASE 

Classification.  —  In  the  following  enumeration,  aortic  disease  will  be 
included  because  histologically  its  intima  is  a  continuation  of  the  endo- 
cardial endothelium,  and  disease  affecting  the  one  often  affects  the 
other. 

Any  classification  adopted  at  this  time  must  in  a  measure  be  arbi- 
trary and  tentative ;  for  example,  diseases  now  grouped  as  toxic  alone 
may  later  be  found  to  be  of  bacterial  origin.  Further  studies  may  isolate 
specific  factors  in  cases  now  grouped  generically.  With  these  limita- 
tions, the  etiology  of  endocarditis  and  of  cardiovascular  disease  may  be 
conveniently  tabulated  as  follows : 


1.  Chemical  Agents  < 


2.  Bacterial  Agents  < 


(a)  Metallic  Poisons. 
(a)  Alcohol. 

(c)  Tobacco. 

(d)  Diabetes. 

(e)  Gout. 

(f)  Products  of  Food  Metabolism. 

(a)  Diphtheria  —  Pneumonia  —  Typhoid  —  Typhus. 
(b)'  Rheumatism  —  Tonsillitis. 

(c)  Pyorrhoea  —  Mouth  Infections. 

(d)  Pyogenic  Abscesses. 


3.  Bacterial  Endocarditis. 

4.  Spirochetal  Infection  —  Cardiovascular  Syphilis. 

1.   Chemical  Agents 

(a)  Metallic  Poisons.  —  Of  these,  the  action  of  lead  is  the  best  known. 
This  metal  attacks  the  endocardium  and  aorta.  In  rare  instances, 
the  coronaries  and  their  branches  also  become  diseased.  The  renal 
arterioles  are  often  involved  and  nephritis  results.  Depending  upon 
the  severity  and  the  location  of  the  arteriolar  disease,  the  symptoms 
and  physical  signs  may  be  those  of  aortitis,  nephritis,  coronary  disease, 
or  of  endocarditis ;  or  there  may  be  a  clinical  picture  combining  these 
pathological  entities  in  varying  proportions.  The  patient's  occupation, 
a  history  of  colic,  peripheral  neuritis,  the  presence  of  a  lead  line  on  the 
gums,  microscopic  examination  of  the  blood,  and  the  chemical  examina- 

149 


150  CLINICAL  CARDIOLOGY 

tion  of  the  feces  and  of  the  total  urine  of  several  successive  days  for  lead 
are  data  which  are  of  aid  in  the  search  for  lead  as  the  etiological  factor. 
Whether  myocardial  degeneration,  when  present,  is  primary  or  is  sec- 
ondary to  disease  of  the  coronary  system  is  still  an  unsettled  question. 
The  selective  action  of  lead  on  the  arterial  system  seems  to  indicate 
that  myocarditis  results  secondarily  from  the  vascular  disease. 

Severe  phosphorus  poisoning  produces  fatty  degeneration  of  the 
heart  and  of  the  arterial  intima.  Other  metallic  poisons  —  copper, 
mercury,  arsenic  —  have  a  much  greater  selective  action  upon  the 
gastro-intestinal  canal,  and  upon  nervous,  osseous,  and  renal,  rather 
than  upon  the  cardiac  structures.  Except  for  the  action  of  mercury 
upon  the  kidneys,  it  is  questionable  whether  these  metallic  poisons 
produce  cardiac  damage  that  is  clinically  recognizable. 

(b)  The  degree  of  damage  to  the  cardiovascular  system  by  alcohol 
is  still  a  matter  of  dispute.  Like  other  poisons,  it  affects  the  cardio- 
vascular structures  to  a  variable  extent,  so  that  necropsy  reports  show- 
ing absence  of  cardiovascular  damage  in  chronic  alcoholism  are  not 
necessarily  evidence  of  its  innocuousness.  It  is  probably  true,  however, 
that  the  importance  and  frequency  of  alcohol  as  a  cardiac  poison  have 
been  overestimated.  Alcohol  attacks  particularly  the  cardiac  mus- 
culature ;  the  result  is  myocardial  disease  varying  from  slight  fatty 
degeneration  to  scar-tissue  formation.  The  arterial  system,  when 
attacked,  presents  various  grades  of  intimal  thickening  and  calcareous 
deposits,  and,  in  exceptional  cases,  degeneration  of  the  remaining 
arterial  coats. 

The  clinical  symptoms  referable  to  alcoholism  are  usually  those  of 
myocarditis  and  of  myocardial  insufficiency.  The  heart  is  moderately 
hypertrophied.  As  a  clinical  syndrome  of  moderate  myocarditis  may 
be  cited  that  due  to  constant  drinking  of  large  amounts  of  beer  (the 
"  Miinchener  Bierherz  ").  In  severe  cases  of  alcoholic  myocarditis, 
cardiac  hypertrophy  may  be  extreme.  In  one  case  that  I  observed  at 
necropsy,  a  man  of  45  who  was  an  inveterate  wine  drinker,  the  ventric- 
ular musculature  consisted  mainly  of  scar  tissue,  the  heart  weighed 
twice  the  normal.  Symptoms  and  clinical  signs  due  to  aortitis  —  an 
impure  first  and  accentuated  second  sound  at  the  right  base,  and  hyper- 
tension —  are  also  occasionally  due  to  alcoholism. 

(c)  Tobacco  Poisoning.  —  It  is  the  general  belief  that  tobacco  users 
are  particularly  prone  to  aortic  disease,  coronary  sclerosis,  and  myo- 
cardial degeneration,  and  that  these  pathological  changes  are  caused 
by  nicotine,  the  main  tobacco  alkaloid.  This  view  is  based  chiefly 
upon  the  result  of  animal  experimentation  consisting  in  the  injection 
of  nicotine  solutions  in  rabbits,  with  the  production  of  a  varying  per- 
centage of  aortitis.  The  injections  must  be  repeated  at  frequent  inter- 
vals over  a  long  period  before  aortitis  results.  As  objections  to  inferences 
drawn  from  these  experiments,  it  must  be  stated  that  others  have  found 
no  abnormal  aortal  change  following  nicotine  injections ;    indeed,  one 


ETIOLOGY  OF  ENDOCARDITIS  151 

observer  found  spontaneous  changes  in  the  aorta  in  a  certain  proportion 
of  normal  rabbits.  Moreover,  it  is  questionable  whether  these  injec- 
tions are  comparable  in  their  effects  to  the  inhalation  of  tobacco  smoke 
in  man.  For  example,  when  the  attempt  was  made  to  produce  parallel 
conditions  by  forcing  rabbits  to  inhale  fumes  on  successive  days  from 
measured  amounts  of  burning  tobacco,  no  definite  changes  in  the  aorta 
were  found.  One  observer  who  made  a  careful  pathological  study  of 
the  hearts  of  heavy  smokers  dying  of  various  diseases  found  only  a 
slight  change  in  the  papillary  muscle;  this  he  attributed  to  the  rapid 
heart  action  usually  found  in  smokers.  From  the  experimental  and 
pathological  sides,  therefore,  it  must  be  concluded  that  no  incontrovert- 
ible proof  has  as  yet  been  adduced  that  smoking  in  itself  produces 
cardiovascular  disease.  On  the  other  hand,  as  the  result  of  physiological 
and  pharmacological  experiments,  it  is  known  that  nicotine  has  a  strong 
neurotropic  action,  particularly  upon  the  sympathetic  nervous  system. 
Many  of  the  symptoms  complained  of  by  patients  with  so-called  '  tobacco 
hearts  '  —  tachycardia,  arrhythmias  of  various  types  (especially  extra- 
systoles),  syncope,  precordial  pains  and  distress  —  can  be  more  readily 
and  rationally  explained,  I  believe,  by  the  selective  action  of  nicotine 
upon  the  sympathetic  nerves  and  ganglia  than  upon  the  assumption 
of  organic  cardiovascular  disease.  In  the  majority  of  cases,  when 
tobacco  is  withdrawn,  cardiac  irregularities  and  pain  cease  and  patients 
examined  months  or  years  later  show  no  evidence  of  organic  damage 
to  the  heart  or  arteries.  I  believe,  however,  that  if  from  any  cause,  a 
tendency  to  aortitis  exists,  its  onset  may  occasionally  be  hastened  by 
tabagism.  Even  this  statement  is  only  surmise,  for  it  is  not  susceptible 
of  clinical  proof. 

(d)  Diabetes  is  frequently  accompanied  by  arteriosclerosis,  ne- 
phritis, and  endocarditis,  less  frequently  by  myocarditis.  These  changes 
are  presumed  to  be  due  to  hyperglycemia  and  to  foreign  chemical  sub- 
stances in  the  blood  which  produce  diminished  alkalinity  (so-called 
acidosis).  The  clinical  symptoms  and  signs  of  the  resultant  cardio- 
vascular disease,  when  not  masked  or  complicated  by  diabetes  itself, 
are  high  blood  pressure,  thickening  of  the  palpable  arteries,  albumen 
and  casts  in  the  urine,  and  aortitis.  The  therapy  should  be  directed 
to  both  diseases  —  diabetes  and  cardiosclerosis ;  relief  or  cure  in  the 
former  is  often  followed  by  beneficial  results  in  the  latter. 

(e)  Gout.  —  Similar  to  diabetes,  gout  is  also  frequently  accompanied 
by  endocardial,  vascular,  and  renal  disease.  An  abnormal  amount 
of  uric  acid  in  the  blood  and  in  the  tissues  may  be  the  cause  of  these 
pathological  changes,  or  both  the  latter  and  gout  may  be  the  expression 
of  some  common,  as  yet  unknown,  underlying  factor  or  diathesis.  The 
problem  of  therapy  directed  to  the  cardiorenal  disease  is  rarely  com- 
plicated by  the  presence  of  gout. 

(/)  Products  of  Food  Metabolism,  Amino  Acids,  etc.  —  The  study 
of  metabolism  and  of  blood  chemistry  has  shown  the  presence  of  amino- 


152  CLINICAL  CARDIOLOGY 

acids  and  other  protein  derivatives  in  the  blood.  Experiments  have 
demonstrated  that  protein  feeding  can  produce  changes  in  the  cardio- 
vascular and  renal  apparatus  of  animals.  Though  clinical  proof  is 
lacking,  these  investigations  suggest  that  protein  overfeeding  in  man 
may  be  followed  by  arterial  disease,  and  that  therefore  proteins  can 
act  as  a  cardiovascular  poison. 

2.  Bacterial  Agents 

In  the  production  of  disease,  bacteria  act  directly,  or  by  the  elabora- 
tion of  chemical  poisons,  i.e.  of  toxins.  The  latter  are  at  present  re- 
garded as  extremely  complex  chemical  poisons  of  nitrogenous  nature. 
It  should  be  remembered  that  the  various  bacterial  agents  attack  dif- 
ferent parts  of  the  cardiac  structure  and  to  a  varying  degree. 

(a)  Diphtheria  Toxins.  —  In  severe  infections,  marked  destruction 
of  the  myocardium  may  result  in  death.  In  one  instance,  a  girl  of  10 
with  severe  diphtheria  and  heart  block,  leucocytic  infiltration  in  the 
junctional  tissue  and  in  the  ventricular  musculature  was  found.  In 
another  instance,  a  child  developed  heart  block  during  the  course  of 
diphtheria.  Electrocardiographic  examination  several  years  later 
still  showed  the  arrhythmia ;  however,  there  were  no  cardiac  symptoms. 
I  have  observed  a  child  8  years  old  with  very  toxic  diphtheria,  in  whom, 
after  a  few  days,  there  were  attacks  of  convulsions  coincident  with  slow 
rhythm.  Polygraphic  tracings  showed  regular  radial  and  ventricular 
activity  at  the  rate  of  40  per  minute ;  the  venous  tracing  was  unsatis- 
factory. Heart  block  was  diagnosed.  The  child  died  one  week  later. 
Necropsy  was  not  obtainable.  From  the  virulent  course  of  the  disease, 
heart  block  seemed  due  to  toxic  degenerative  myocarditis. 

Milder  toxic  destruction  of  the  myocardium  is  evidenced  by  the  usual 
signs  of  myocardial  insufficiency,  especially  by  dyspnoea.  Other  evi- 
dence is  the  presence  of  arrhythmias :  —  heart  block,  auricular  and 
ventricular  extrasystoles,  auricular  fibrillation,  tachycardia .  These  types 
may  frequently  interchange.  They  are  apparently  indicative  of  myo- 
cardial degeneration.  Pathologically,  the  muscle  cells  undergo  fatty 
degeneration,  the  valves  and  endocardium  are  rarely  involved.  With 
reference  to  the  arrhythmias  it  must  be  remembered  that,  as  in  other 
acute  febrile  and  infectious  diseases,  cardiac  irregularities  may  occur  in 
diphtheria  at  the  onset  or  crisis,  without  any  evidence  of  cardiovascular 
degeneration.  Such  irregularities  at  these  times  are  probably  the  effect 
of  toxins  on  the  normal  neurogenic  cardiac  control ;  they  are  harmless 
and  rarely  require  medication.  It  is  therefore  important  to  differentiate 
the  innocuous  from  the  dangerous  arrhythmias  in  diphtheria.  With  our 
present  knowledge,  this  is  best  accomplished  by  a  careful  and  complete 
examination  of  the  entire  cardiovascular  apparatus,  and  not  alone  by 
a  consideration  of  the  types  of  arrhythmias.  The  presence  of  cardiac 
failure,  slight  or  severe,  —  dyspnoea,  cyanosis,  edema,  cardiac  dilata- 


ETIOLOGY  OF  ENDOCARDITIS  153 

tion  —  indicates  that  any  type  of  irregularity,  except  physiological 
sinus  arrhythmia,  is  of  serious  or  even  ominous  import. 

The  study  of  the  heart  in  diphtheria  is  further  complicated  by  the 
occasional  occurrence  of  unexpected,  sudden  death.  This  is  usually 
regarded  as  due  to  cardiac  paralysis.  Some  of  these  deaths  can,  I 
believe,  be  explained  upon  the  assumption  of  a  destructive,  progressive 
myocardial  degeneration  with  slight  or  no  symptoms  during  life,  or 
with  the  cardiac  symptoms  masked  by  those  due  to  the  diphtheria 
itself.  In  other  cases,  in  which  myocardial  damage  is  not  demonstrated 
at  necropsy,  these  fatalities  may  possibly  be  regarded  as  anaphylactic 
phenomena  affecting  the  cardio-inhibitory  center  or  the  intracardiac 
nerve  supply. 

Pneumonia.  —  In  pneumonia  pneumococci  are  not  infrequently 
found  in  the  circulating  blood.  The  manner  in  which  the  myocardium 
is  damaged  is  still  in  dispute.  I  am  of  the  opinion  that  the  myocardial 
damage  is  usually  the  result  of  toxemia.  This  is  to  some  extent  based 
upon  the  observation  of  two  cases  of  heart  block  that  occurred  during 
pneumonia.  One,  a  man  of  70,  came  to  necropsy.  Macroscopical 
examination  of  the  brain  and  spinal  cord  and  microscopical  examination 
of  the  heart,  including  the  junctional  tissues,  showed  that  all  these 
structures  were  normal.  Another  case,  a  man  of  50,  entered  the  hospital 
in  collapse  and  semi-stupor.  The  temperature  was  104°.  There  was 
pneumonic  consolidation  of  the  left  upper  lobe.  The  temperature 
ranged  between  100°  and  104°  for  one  week.  The  heart  sounds  were 
scarcely  audible,  the  radial  pulse  was  regular,  its  rate  between  100  and 
120  per  minute.  At  the  end  of  one  week,  there  was  critical  defervescence, 
the  temperature  fell  to  97.4°  per  rectum,  there  was  extreme  collapse. 
The  ventricular  rate  suddenly  dropped  to  44,  and  remained  between 
30  and  44  for  four  days.  Although  satisfactory  graphic  records  could 
not  be  obtained,  heart  block  was  diagnosed  by  the  clinical  phenomena 
and  pulse  rate.  The  pneumonic  area  underwent  gradual  resolution. 
There  were  no  general  convulsions,  but  frequent  convulsive  tremors 
of  the  musculature  of  the  upper  and  lower  extremities.  The  stupor 
slowly  deepened  into  coma.  Suddenly,  one  week  after  the  inception 
of  the  slow  rhythm,  the  patient  sat  up  in  bed  fully  oriented,  with  good 
color,  warm  extremities,  and  a  pulse  and  ventricular  rate  of  76  per 
minute.  The  heart  sounds,  though  still  faint,  were  readily  heard. 
Except  for  two  occasions  a  few  days  later,  the  pulse  continued  regular. 
From  its  occurrence  with  critical  defervescence  and  its  continuance 
during  resolution,  the  cause  of  heart  block  seemed  due  to  toxins  liberated 
at  the  crisis  and  affecting  the  inhibitory  cardiac  control. 

Action  of  Pneumonia  on  the  Heart  during  the  Acute  Process  and  as 
a  Late  Sequela.  —  Endocarditis  due  directly  to  an  invasion  by  pneu- 
mococci is  by  no  means  rare ;  this  type  will  be  discussed  later.  Many 
pathological  examinations  of  the  effect  of  pneumonia  on  the  cardiac 
musculature  have  been  reported.     Slight  degeneration  (cloudy  swelling) 


154  CLINICAL  CARDIOLOGY 

has  been  the  rule ;  occasionally  more  severe  damage  has  been  described. 
^Yhen  widespread,  these  degenerative  changes  can  undoubtedly  cause 
death.  But  there  is  no  evidence  that  slight  cardiac  degeneration,  the 
usual  change  in  pneumonia,  is  in  itself  sufficient  to  produce  death ;  nor 
have  attempts  been  made  to  correlate  the  amount  and  degree  of  path- 
ological damage  with  the  clinical  or  bacteriological  evidence  of  toxicity. 
Experimental  evidence  pertaining  to  this  subject  indicates  that  pneu- 
monia usually  acts  as  a  poison  upon  the  functional  power  of  the  heart ; 
for  example,  pneumonic  blood  perfused  into  a  healthy  dog's  heart  is 
immediately  followed  by  very  much  weakened  contractility.  The 
contractions  become  normal  when  healthy  blood  is  subsequently  per- 
fused. At  present  the  conclusion  seems  warranted  that  death  from 
pneumonia  in  the  majority  of  cases  is  not  due  to  demonstrable  changes 
in  the  myocardium.  On  the  other  hand,  damage  to  the  cardiovascular 
apparatus  as  a  late  sequel  of  pneumonic  infections  has  been  insufficiently 
emphasized.  Such  sequelae  produce  symptoms  only  some  months  or 
years  after  the  pneumonia  has  run  its  course,  so  that  the  connection 
between  the  two  diseases  is  often  entirely  overlooked.  In  some  instances 
the  pneumonic  poison  seems  to  light  up  a  dormant  cardiovascular  pro- 
cess ;  in  others,  it  primarily  produces  this  condition.  Brief  case  reports 
of  both  types  are  herewith  given : 

Male,  age  50,  entered  the  hospital  with  a  mild  pneumonia.  He 
recovered  within  one  week.  The  only  point  of  interest  in  a  careful 
examination  of  the  cardiovascular  system  was  a  slightly  accentuated 
second  sound  over  the  right  base,  suggestive  of  aortitis.  The  Wasser- 
mann  blood  reaction  was  negative.  The  urine  and  the  blood  pressure 
were  normal.  Two  months  later  the  patient  reentered  the  hospital 
with  the  history  of  a  pneumonic  attack  three  weeks  before.  He  pre- 
sented all  the  typical  evidence  of  cardiosclerosis  with  decompensation: 
—  anasarca,  urine  containing  albumen  and  casts,  high  blood  pressure, 
markedly  accentuated  second  aortal  sound.  Evidences  of  the  recent 
pneumonia  were  still  present. 

A  physician,  age  50,  had  for  several  years  remarked  occasional 
dyspnoea  upon  walking  but  never  considered  himself  ill.  Two  years 
before  coming  under  observation,  he  developed  a  severe  pneumonia 
which  ran  a  toxic  course  and  lasted  several  weeks.  A  few  months 
thereafter,  cardiac  symptoms  began.  He  became  dyspnoic  and  edema- 
tous. Hypertension  developed.  The  urine  containen  albumen  and 
casts.  Orthodiascope  examination  one  year  later  showed  marked 
enlargement  of  the  aortic  arch  and  of  the  left  ventricle.  With  some 
remissions,  the  cardiac  symptoms  lasted  until  the  time  of  his  death,  one 
year  and  a  half  later. 

Both  these  cases  illustrate  the  effect  of  pneumonia  upon  what  seemed 
otherwise  quiescent  cardiovascular  disease. 

Male,  aged  32,  never  drank  or  smoked.  He  had  a  grippe  infection 
with  fever  six  years  previously ;  this  lasted  several  months ;  pulmonary 


ETIOLOGY  OF  ENDOCARDITIS  155 

tuberculosis  was  suspected  but  bacilli  were  never  found.  Cardio- 
nephritic  symptoms  began  three  years  later.  They  were  at  first  mild 
and  consisted  of  occasional  dyspnoea  when  climbing  stairs.  The  signs 
of  cardiosclerosis  gradually  progressed  so  that  at  the  time  of  examina- 
tion, although  the  patient  complained  only  of  slight  dyspnoea  and  pre- 
cordial pain,  the  left  half  of  the  chest  was  practically  filled  by  a  hugely 
hypertrophied  heart.  The  systolic  blood  pressure  ranged  between 
250  and  300  mm.  of  mercury,  the  first  sounds  at  the  right  base  and  at 
the  apex  were  exceedingly  harsh  and  rough,  indicative  of  probable  cal- 
cification of  the  mitral  valves  and  aorta.  The  second  sound  at  the 
right  base  was  markedly  accentuated ;  the  urine  contained  albumen 
and  casts.  The  Wassermann  blood  reaction  was  negative.  The  clinical 
picture  was  that  of  extremely  advanced  cardiosclerosis  and  nephritis. 

From  the  history  and  from  the  absence  of  other  etiological  factors, 
it  is  fair  to  conclude  that  the  pulmonary  infection  six  years  before  the 
onset  of  symptoms  was  the  direct  and  only  cause  of  the  cardiovascular 
disease. 

The  action  of  diphtheria  and  of  pneumonia  as  cardiovascular  poisons 
has  been  described  in  some  detail  because  similar  observations  apply 
in  varying  degrees  to  other  infectious  diseases.  Typhoid  fever  deserves 
special  mention  in  this  connection.  Therefore,  careful  search  for  such 
etiological  factors  should  be  made  in  every  case  of  cardiac  and  arterial 
disease  in  which  the  cause  is  obscure. 

(6)  Rheumatism  —  Tonsillitis.  — Of  all  diseases,  rheumatism  is  the 
most  frequent  cause  of  valvular  disease.  Although  the  etiology  of 
rheumatism  is  not  as  yet  known,  recent  experimental  research  and 
clinical  observation  indicate  that  it  is  of  bacterial,  probably  of  strep- 
tococcic, origin.  For  the  present,  however,  it  is  here  classified  under 
Toxemias.  Valvular  endocarditis  is  the  most  frequent  sequel  of  a 
rheumatic  infection.  Myocarditis,  which  follows  less  frequently, 
usually  occurs  in  the  form  of  submiliary  inflammatory  nodes  (Aschoff 
bodies).  Permanent  damage  always  results  from  rheumatic  valvulitis 
and  myocarditis ;  but  here,  as  elsewhere  in  the  body,  if  the  infective 
process  stops  early,  scar  tissue  may  form  before  clinical  signs  of  myo- 
cardial or  valvular  disease  present  themselves.  The  necropsy  alone 
gives  evidence  of  cardiac  damage  in  such  instances.  Even  if  clinical 
manifestations  are  present,  particularly  in  cases  of  mitral  regurgitant 
lesions,  the  process  may  heal,  so  that  valvular  leakage  stops  and  the 
patient  remains  clinically  well.  Such  observations  have  been  sub- 
stantiated by  post-mortem  examination. 

Tonsillitis  is  grouped  with  rheumatism  in  the  etiology  of  cardiac 
disease,  for  it  gives  rise  to  joint  manifestations  and  to  endocarditis, 
similar  to  rheumatism.  Even  without  joint  involvement,  tonsillitis 
frequently  causes  endocarditis.  In  fact,  exceedingly  mild  and  ap- 
parently harmless  tonsillar  and  pharyngeal  attacks,  accompanied  by 


156  CLINICAL  CARDIOLOGY 

a  few  minute  spots  on  the  tonsils  or  pharynx,  can  be  the  source  of 
an  endocardial  infection.  For  example,  a  vigorous  young  man  of  21 
developed  mild  pharyngeal  grippe  lasting  three  days;  the  highest 
temperature  was  101.5°.  Within  one  week  typical  signs  of  a  mitral 
regurgitant  lesion  were  present.  Similarly  so-called  '  colds  '  —  acute 
pharyngeal  and  nasal  catarrh  —  can  be  the  infectious  nidus  for  endo- 
carditis. 

(c)  Pyorrhoea  Alveolaris.  —  Much  experimental  and  clinical  work 
has  recently  been  done  to  show  that  the  various  organisms  harbored 
in  the  mouth  and  producing  pyorrhoea  may,  by  systemic  absorption, 
cause  endocarditis  and  myocarditis.  Among  other  bacteria,  the  strep- 
tococcus viridans  has  been  especially  accused.  However,  it  has  been 
shown  that  this  organism  is  a  fairly  frequent  inhabitant  of  the 
normal  mouth ;  hence  not  only  demonstration  of  the  pyogenic  organ- 
ism is  required  but  also  definite  clinical  evidence  that  it  bears  an 
etiological  relationship  to  the  cardiac  disease.  In  the  face  of  negative 
blood  cultures  and  in  view  of  the  other  well-known  causes  for  endo- 
carditis, the  correlation  between  pyorrhoea  alveolaris  and  cardiac 
disease  can  only  be  established  by  a  thorough  examination  of  the 
mouth  for  carious  teeth,  for  periostitis,  and  for  pyorrhoea,  and  by 
radiographic  examination  of  the  roots  of  the  teeth  for  evidence  of 
absorption  and  caries.  This  constitutes  the  first  step.  Then  a 
careful  search  of  the  entire  body  must  be  made  for  other  possible 
infective  foci  which  may  cause  cardiovascular  disease.  Cholecystitis, 
cystitis,  deep-seated  bone  abscess,  pyelitis  are  some  of  these  bacterial 
conditions.  So  that  even  should  roentgenography  disclose  root  ab- 
scesses, and  the  mouth  harbor  pathogenic  bacteria,  it  is  for  the  clinician 
to  decide  from  the  clinical  history,  the  type  and  probable  duration  of 
the  cardiovascular  disease,  and  from  a  complete  examination  for  all  other 
possible  sources  of  infection,  what  weight,  etiologically,  should  be 
given  to  the  presence  of  root  abscesses  as  the  causative  agent  of  endo- 
carditis. Thus  studied,  it  appears  to  me  that  the  claims  now  made  for 
the  extremely  frequent  connection  between  oral  infections  and  heart 
disease  will  be  found  unwarranted.  This  statement  indeed  fits  in  with 
general  clinical  experience.  Very  many  children  with  valvular  disease 
possessing  healthy  teeth  have  been  observed  as  well  as  very  many  with 
carious  teeth  and  normal  hearts.  In  those  patients  with  cardiovascular 
disease  observed  by  me,  in  whom  extraction  of  teeth  had  been  done 
because  of  root  abscesses,  there  was  no  effect  upon  the  cardiovascular 
process  or  upon  the  clinical  signs.  One  would  not  expect  the  small 
amount  of  toxins  presumably  elaborated  and  absorbed  from  a  small 
dental  focus  to  be  a  frequent  cause  of  endocarditis ;  one  would  expect 
sufficient  anti-bodies  to  be  developed  to  prevent  cardiac  mischief  in 
the  great  majority  of  cases.  On  the  other  hand,  it  cannot  be  denied 
that,  in  an  extremely  susceptible  individual,  general  systemic  damage 
and  cardiac  disease  can  thus  occasionally,  though  I  believe  only  very 


ETIOLOGY  OF  ENDOCARDITIS  157 

rarely,  be  produced.  It  is,  therefore,  necessary  for  the  clinician  to 
weigh  all  factors  and  not  to  conclude  too  hastily  that  because  pus,  path- 
ological bacteria,  or  small  root  abscesses  are  found  in  the  mouth  they 
are  necessarily  the  cause  of  the  cardiovascular  disease  in  that  individual. 
We  are  greatly  indebted  to  the  dental  profession  for  indicating  the 
teeth  as  a  cause  of  endocarditis,  but  the  physician  must  finally  judge 
all  the  evidence  in  every  case  before  he  can  decide  whether  the  cause 
of  endocarditis  lies  in  the  mouth  or  elsewhere.  None  of  the  statements 
here  made  of  course  militate  against  the  fact  that  purulent  mouth  condi- 
tions should  be  carefully  treated,  or  that  children  with  diseased  teeth 
should  receive  proper  dental  attention  in  order  to  remove  that  source  of 
a  possible  endocarditis.  My  main  object  has  been  to  refute  the  now 
widely  accepted  opinion  that  diseased  teeth  commonly  cause  disease  of 
the  heart.  In  those  exceptional  cases  under  my  observation  in  which 
alveolar  pyorrhoea  was  apparently  the  cause  of  the  existent  cardio- 
vascular disease,  the  pyorrhoea  was  frank  and  usually  severe  even  to  the 
time  that  the  patients  presented  themselves  for  examination  because  of 
cardiac  symptoms.  There  was  usually  a  long  history  of  foul  breath 
and  of  decaying  and  loose  teeth.  The  patients  were  of  middle  age 
or  past  middle  age.  When  brought  out  by  questioning,  the  history 
of  pyorrhoea  was  definite  and  of  several  years'  duration.  Of  extreme 
interest  and  importance  is  the  fact  that,  symptomatically  and  patho- 
logically, the  picture  is  usually  that  of  cardiosclerosis  (q.v.).  It 
seems  as  if  the  toxin  acts  primarily  upon  the  arterioles  of  the  cardio- 
vascular system,  affecting  in  varying  degrees  the  vessels  of  the  heart 
and  kidneys.  Its  final  effect  upon  these  organs  often  closely  resembles, 
indeed  sometimes  coincides  with,  the  pathological  picture  of  senile 
cardiosclerosis  (q.v.). 

(d)  Pyogenic  Abscesses. — These  may  occasionally  produce  endo- 
carditis by  the  production  of  a  bacteremia  or  from  toxins.  In  endo- 
carditis, where  a  frank  etiological  factor  cannot  be  found,  careful 
search  should  be  made  for  hidden  abscesses  as  possible  causes. 


3.   Bacterial  Endocarditis 

Bacteria  were  demonstrated  in  valvular  vegetations  by  Heiberg 
as  early  as  1869.  Since  then,  many  types  of  organisms  have  been  re- 
covered from  such  vegetations,  and,  more  recently,  have  been  isolated 
from  the  blood. 

The  question  of  systemic  bacterial  infection  in  rheumatic  fever  is 
still  unsettled,  although,  as  already  indicated,  there  are  good  clinical 
and  experimental  grounds  for  considering  it  a  bacterial  disease.  The 
organisms  found  in  the  blood  which  produce  endocarditis  are  grouped, 
according  to  Simons'  modification  of  Litten's  classification,  as  fol- 
lows: 


158  CLINICAL  CARDIOLOGY 


'  Streptococcus  viridans  (Schottmuller). 

Endocarditis  cocci  (Libman). 

Modified  pneumococci  (Rosenow). 

Saprophytic  Streptococci  (Horder). 
.  Streptococcus  tenuans  (Hastings). 


1.  Ordinary  Streptococcus. 

2.  Small  Streptococcus.     (Probably 

all  alike,  but  variously  named 
by  different  observers.) 

3.  Staphylococcus  albus  and  aureus. 

4.  Pneumococcus. 

5.  Gonococcus. 

6.  Meningococcus. 

7.  Bac.  coli. 

8.  Bac.  influenzae. 

9.  Bac.  pyocyaneus. 

From  the  statistics  of  various  authors,  the  most  common  invaders 
in  acute  bacterial  infections  are,  in  the  order  of  their  frequency,  the 
streptococcus  pyogenes  and  the  staphylococcus  aureus ;  fairly  frequent 
are  the  pneumococcus  and  gonococcus ;  the  streptococcus  viridans  is 
very  rare.  The  other  bacteria  —  staphylococci,  meningococci,  bac. 
coli,  bac.  pyocyaneus,  and  bac.  aerog.  capsulat.  —  are  only  occasionally 
found.  The  chronic  invaders  are,  in  the  order  of  frequency,  the  strep- 
tococcus viridans  (which  is  very  common),  the  streptococcus  pyogenes, 
pneumococcus,  bac.  influenzae,  and  the  gonococcus.  It  is  thus  seen  that 
the  gram-positive  chain  cocci  are  the  chief  causes  of  bacterial  endo- 
carditis. 

Relative  Frequency  of  the  Bacterial  Invasions  and  of  the  Valvular 
Affections.  —  The  mitral  is  the  valve  most  frequently  affected  alone ; 
next  in  frequency  is  the  aortic.  Bacterial  infection  of  the  pulmonary 
or  tricuspid  valves  alone  is  exceedingly  rare.  The  most  common 
combination  of  a  multiple  infection  is  the  mitral  and  aortic ;  the  next, 
the  tricuspid  and  mitral.  Vegetations  on  the  walls  of  the  auricle 
and  ventricle  have  also  been  described,  but  they  do  not  occur  without 
vegetations  on  the  valves  as  well.  The  pathological  features  of  chronic 
streptococcus  viridans  are  discussed  in  connection  with  the  clinical 
features  of  that  affection  (q.v.). 


4.   Spirochetal  Infection 

The  immense  strides  made  possible  in  the  detection  of  syphilis  by  the 
discovery  of  the  causative  organism  (spirocheta  pallida),  and  by  the  use 
of  the  Wassermann  reaction,  have  enhanced  our  knowledge  of  the  fre- 
quency of  lues  as  a  cause  of  cardiac  disease.  The  relation  of  syphilis  to 
valvular  disease,  especially  to  disease  of  the  aorta,  although  not  proven, 
had  long  been  suspected.  Syphilis  has  now  been  demonstrated  as  a 
very  common  cause  of  disease  of  the  heart  muscle ;  in  fact,  myocarditis 
is  occasionally  present  in  the  secondary,  as  well  as  in  the  tertiary,  stages 
of  lues.  By  special  staining  methods,  the  spirochete  has  been  found 
in  the  aorta  and  in  the  cardiac  musculature.  The  most  marked,  and 
probably  the  earliest,  pathological  involvement  consists  in  a  periarteritis 


ETIOLOGY  OF  ENDOCARDITIS  159 

of  the  arterioles  of  the  coronary  system,  resulting  in  various  types  of 
muscle  degeneration  (fibrosis,  fatty  degeneration,  brown  atrophy). 
As  a  later  involvement,  gumma  and  gummatous  infiltrations  also  occur. 
The  valves  and  walls  of  the  aorta  are  the  most  common  situation  for 
cardiovascular  syphilis.  The  picture  varies  from  mild  arteriosclerosis 
to  extreme  cicatrization  with  calcification.  Thickening  of  the  mitral 
cusps  is  less  frequent.  It  may,  however,  be  sufficient  to  produce  signs 
of  a  mitral  regurgitant  lesion.  Endocardial  changes  varying  from  slight 
opacities  to  extensive  degeneration  may  coexist. 


CHAPTER  XII 

PATHOLOGY   OF   THE   ENDOCARDIUM    AND   MYOCARDIUM, 
AND   OF   CARDIOSCLEROSIS 

Structure  of  the  Endocardium.  —  The  endocardium  is  composed 
of  connective  tissue  containing  smooth  muscle-  and  elastic  fibers;  its 
free  surface  is  covered  by  a  layer  of  endothelial  cells.  Underneath 
this  layer  is  one  of  loose  areolar  tissue  continuous  with  the  intermuscu- 
lar connective  tissue  septa ;  this  stratum  also  contains  the  blood  vessels. 
The  cardiac  valves  are  composed  of  fibrous  connective  tissue  covered 
by  endocardium ;  they  contain  muscle  fibers  at  their  attached  margins. 
The  normal  semilunar  valves  have  no  blood  vessels ;  the  normal  tri- 
cuspid and  mitral  valves  contain  blood  vessels  only  in  the  muscular 
tissue  at  their  bases,  the  muscular  tissue  being  a  reflected  layer  of  vary- 
ing size  from  the  main  ventricular  mass. 

In  the  description  of  the  different  pathological  varieties  of  endo- 
and  myocardial  changes,  the  classification  given  by  E.  Kaufmann  will 
in  the  main  be  followed. 

The  endocardium  is  subject  to  the  following  degenerative  changes : 

Fatty  Degeneration.  —  Macroscopically,  pure  or  yellowish  white 
areas  are  found  in  the  endocardium,  especially  on  the  mitral  valves  in 
old  people.  Such  degenerative  areas  usually  represent  senile  changes ; 
they  are,  however,  occasionally  the  result  of  anemia,  toxemias,  and 
infections. 

Sclerosis.  — The  affected  endocardium  takes  on  a  white,  thickened, 
and  hyaline  appearance.  An  entire  valve,  especially  the  mitral,  its 
free  border,  or  parts  of  the  mural  endocardium,  may  be  involved;  in 
addition  to  these  changes  there  may  be  calcareous  deposits.  Occasionally 
the  sclerotic  areas  undergo  mucoid  degeneration.  Microscopically, 
the  sclerotic  patches  are  found  to  consist  of  strands  of  connective  tissue 
which  have  undergone  hyaline  degeneration. 

Atheromatous  Degeneration. — This  consists  of  focal  necrosis  in  the 
valvular  tissue  and  may  include  any  of  the  changes  already  mentioned. 

The  above  degenerative  types  are  as  a  rule  found  in  elderly  people, 
and  may  be  regarded  as  senile  in  nature.     They  are  occasionally  encoun- 

160 


PATHOLOGY  OF  THE   ENDOCARDIUM  161 

tered  in  the  middle  aged,  very  rarely  in  the  young.  The  valves  especially 
attacked  by  these  degenerative  processes  are  those  previously  inflamed. 
The  result  is  that  the  free  surface  of  the  valvular  endocardium  becomes 
roughened ;  adherent  thrombi  may  form  which  later,  following  a  slow 
productive  inflammation,  become  partially  or  totally  organized.  Thick- 
ened patches  are  thus  formed.  The  end  result  of  all  these  changes 
is  an  irregular,  more  or  less  diffuse,  sclerotic,  and  atheromatous  thick- 
ening of  the  valves,  with  consequent  profound  change  in  their  structure, 
shape,  and  function.  They  can  no  longer  close  the  cardiac  orifices 
properly,  thus  giving  rise  to  various  abnormal  blood  currents  and  to 
murmurs  (Chapter  X). 

It  is  at  times  difficult  to  differentiate  this  primary  sclerosis  and 
atheroma  from  chronic  fibrous  and  infectious  endocarditis. 

Endocarditis,  sometimes  called  thrombo-endocarditis  because  of 
its  chief  pathological  feature,  is  an  inflammation  involving  the  valves 
and  occasionally  also  the  mural  endocardium  and  chordae  tendinese. 
As  discussed  in  another  connection  (Chapter  XI)  endocarditis  may  be 
produced  by  bacteria,  their  toxins,  or  by  foreign  chemical  substances 
flowing  in  the  general  circulation.  In  bacterial  endocarditis  (i.e.  where 
quantities  of  bacteria  are  found  in  the  circulating  blood)  the  usual 
sequence  of  the  pathological  process  affecting  the  valves  is  as  follows : 
The  bacteria  form  clump-like  deposits  which  appear  as  very  fine  grayish 
granules.  Beneath  these,  there  is  destruction  and  necrosis  of  the 
endothelial,  and  finally  of  the  deeper  layers  of  the  valvular  structure. 
The  extent  of  the  destructive  process  apparently  depends  upon  the 
virulence  of  the  invading  bacteria.  If  the  endothelial  layer  is  not 
entirely  destroyed,  it  shows  only  cloudy  swelling.  Thrombi  from  the 
circulating  blood,  consisting  of  platelets,  fibrin,  and  white  and  red  blood 
cells,  become  adherent  to  the  damaged  surface.  With  the  washing  off 
of  the  bacterial  clumps  by  the  blood  stream  there  remains  a  small  defect 
with  a  necrotic  base,  to  which  thrombi  again  become  attached.  Where 
blood  vessels  are  present  in  the  valves,  an  exudative  inflammation  sur- 
rounds the  necrotic  areas.  Where  the  vascular  supply  is  absent  there 
is  a  growth  of  connective  tissue  cells  and  an  increase  in  lymphocytes ; 
later,  there  may  be  formation  of  new  blood  vessels.  In  acute  foudroyant 
cases,  also  called  ulcerative,  malignant,  or  septic  endocarditis,  in  which 
there  is  extreme  bacterial  virulence  with  large  bacterial  deposits  on  the 
valves,  the  necrosis  spreads  to  the  deeper  layers.  This  is  due  to  the 
primary  effect  of  the  bacteria  or  their  toxins,  or  is  secondary  to  an  in- 
tense purulent  inflammation.  In  this  manner,  large  valvular  defects 
are  soon  produced.  In  less  virulent  subacute  and  chronic  cases,  there 
is  connective  tissue  production  of  flat  wart-like  excrescences  upon  the 
valves.  This  process  has  been  variously  termed  verrucous,  productive, 
simple,  or  rheumatic  endocarditis.  The  damage  is  occasionally  so 
mild  and  superficial  that  the  only  sign  of  a  previous  inflammation  is 
a  small  amount  of  scar  tissue.     Since  the  verrucous  and  ulcerative 


162  CLINICAL  CARDIOLOGY 

varieties  of  endocarditis  are  not  always  distinct,  and  may  merge  into 
each  other,  they  may  both  occur  together  as  a  mixed  process.  A  shrink- 
age of  the  granulomatous  connective  tissue  produces  what  is  known  as 
chronic  fibrosis  or  fibroplastic  endocarditis. 

Verrucous  endocarditis  is  usually  found  in  the  left  heart  in  adults. 
The  ulcerative  type  is  seen  fairly  frequently  in  the  right  side  of  the 
heart.  In  the  new  born,  the  site  of  predilection  for  verrucous  endo- 
carditis is  also  the  right  heart. 

The  verrucse  and  the  formation  of  fibrous  tissue  give  rise  to  stenoses 
of  the  valvular  orifices  (Stenotic  lesions,  Chapter  X),  or  the  valves  no 
longer  properly  close  the  orifices,  they  became  incompetent  and  allow 
the  blood  to  flow  back  into  abnormal  cardiac  chambers  (Regurgitant 
lesions,  Chapter  X). 

It  is  of  importance  to  correlate,  where  possible,  the  pathological 
picture  of  endocarditis  with  valvular  disease  as  encountered  clinically. 
Thus,  in  acute  endocarditis,  the  usual  change  consists  in  the  production 
of  ulcers  with  thickening  of  the  cusps,  and  the  presence  of  healed  areas 
and  of  granulations.  Valvular  deformity  is  slight  or  absent.  In  the 
longer  continued,  subacute  cases  of  endocarditis,  verruca?  along  the  mar- 
gins of  the  valves  represent  the  prominent  pathological  change.  Vak 
vular  deformity  is  moderate.  In  chronic  endocarditis,  there  is  produc- 
tion of  new  tissue  affecting  not  only  the  valves  but  also  the  chordae 
tendinse ;  the  latter  become  stiff,  the  valves  hard  and  inelastic.  The 
result  of  both  of  these  changes  is  marked  deformity ;  in  the  case  of  the 
mitral  valves,  there  is  lengthening  and  funnel-like  formation  of  the 
mitral  opening,  accompanied  by  varying  degrees  of  stenosis. 

Myocardium 

The  following  are  the  chief  pathological  changes  occurring  in  the 
myocardium. 

Simple  and  Brown  Atrophy.  —  In  both,  the  cardiac  fibers  become 
smaller  and  the  entire  heart  is  decreased  in  size.  In  addition,  in 
brown  atrophy  pigment  is  found  as  small  granules  in  the  sarcoplasm. 
The  entire  heart  presents  a  brownish  appearance.  Both  types  occur 
in  inanition,  and  in  various  cachectic  states.  Brown  atrophy  especially 
is  regarded  as  a  senile  change. 

Parenchymatous  Degeneration.  —  Microscopically,  this  is  marked 
by  cloudy  swelling.  Macroscopically,  the  cardiac  musculature  has  an 
opaque,  dark  red,  somewhat  spotted  appearance,  and  is  softer  and  more 
friable  than  the  normal  muscle.  This  degenerative  change  is  a  frequent 
accompaniment  of  infectious  fevers  and  of  biological  and  chemical 
poisons.     It  is  also  found  in  severe  anemia. 

Fatty  Degeneration.  —  This  exists  as  a  primary  process  or  represents 
a  later  development  of  parenchymatous  degeneration.  Depending 
upon  its  severity,  the  myocardium  is  studded  with   fat   droplets   of 


PATHOLOGY  OF  THE   ENDOCARDIUM  163 

various  size.  Macroscopically,  the  musculature  shows  patchy  or 
diffuse  yellowish  areas.  When  the  damage  is  extreme,  the  mus- 
cle is  flabby,  friable,  and  grayish  in  color.  Very  many  factors,  espe- 
cially those  that  alter  the  quantity  and  quality  of  the  blood,  may 
cause  fatty  degeneration.  For  example,  it  is  found  in  severe  primary 
anemias,  in  anemia  following  hemorrhage,  in  infectious  diseases,  in 
chemical  intoxications  (especially  from  phosphorus,  arsenic  and  alcohol), 
in  coronary  disease,  in  cardiac  hypertrophy,  and  in  chronic  nephritis. 

The  "  Fatty  "  Heart.  —  Fatty  degeneration  must  be  distinguished 
from  what  is  ordinarily  termed  the  "  fatty  heart."  In  the  latter 
the  organ  is  covered  by  more  or  less  extensive  fat  pads.  Some- 
times these  lipomatous  masses  insinuate  themselves  between  muscle 
bundles  and  appear  as  fat  clumps  or  spots  under  the  endocardium.  "  Fatty 
hearts  "  are  usually  the  accompaniment  of  fat  accumulations  in  other 
parts  of  the  body,  in  obese  and  thickset  individuals ;  very  rarely  these 
masses  are  found  as  secondary  changes  in  the  cardiac  atrophy  of  cachexia. 

Disturbances  of  the  circulation  sometimes  give  rise  to  myocardial 
changes.  This  is  especially  true  of  focal  anemia  subsequent  to  inter- 
ference with  the  coronary  circulation  from  emboli  in  the  main  cor- 
onaries  or  their  subsidiaries,  or  from  coronary  endarteritis.  Either  of 
these  impedes  or  entirely  stops  the  intrinsic  arterial  supply.  Coronary 
endarteritis  causes  extreme  intimal  thickening  or  calcareous  deposits ; 
thrombi  may  become  adherent  to  the  denuded  roughened  intimal  surface. 

Anemic  Necrosis.  —  Following  complete  obliteration  of  one  of  the 
smaller  coronaries,  the  corresponding  cardiac  area  becomes  ischemic 
and  pale,  and  undergoes  coagulation  necrosis,  a  process  sometimes 
termed  anemic  necrosis  or  anemic  infarct.  The  infarcted  area  may 
become  myomalacious.  In  rare  instances,  such  softened  areas  develop 
into  aneurisms  of  the  cardiac  wall  which  may  finally  rupture.  A  more 
frequent  outcome  is  organization  of  the  anemic  infarct ;  the  necrotic 
material  is  absorbed,  and  vascularized  granulation  tissue  takes  its  place. 
This  ends  in  fibrous  or  fibroplastic  myocarditis,  and,  finally,  in  scar 
tissue  formation.  If  the  process  is  widespread,  the  ventricular  mus- 
culature appears  striped  on  section.  It  presents  a  somewhat  checkered 
appearance  if  older  scars  are  found  in  conjunction  with  fresh  necrotic 
areas. 

Acute  Interstitial  Myocarditis.  —  As  the  result  of  bacterial  infection, 
in  which  a  clump  forms  the  inflammatory  nidus,  an  area  of  cloudy  swell- 
ing, necrosis,  and  fatty  degeneration  of  the  musculature  is  developed. 
The  necrotic  area  becomes  infiltrated  by  a  zone  of  leucocytes.  If  the 
leucocytes  penetrate  the  necrotic  zone,  an  abscess  results.  These 
abscesses  are  usually  minute,  though  by  confluence  they  may  sometimes 
be  readily  seen  by  the  naked  eye.  Small  abscesses  end  in  scar  tissue 
formation  by  destruction  of  bacteria  and  liquefaction  and  absorption 
of  the  pus  cells.  The  defect  is  then  covered  by  granulation  tissue 
coming  from  the  surrounding  musculature.     On  the  other  hand,  these 


164  CLINICAL   CARDIOLOGY 

foci  may  cause  purulent  pericarditis,  emboli,  ulcerative  myocarditis, 
and  cardiac  aneurisms.  Any  of  these  sequelae  can  directly  or  indirectly 
cause  death.  In  those  instances  in  which  the  inflammation  stops  short 
of  abscess  formation,  the  process  may  end  in  the  production  of  granu- 
lation, of  young  connective  and,  finally,  of  scar  tissue.  This  occurs 
especially  in  the  myocarditis  accompanying  rheumatic  endocarditis 
in  which  large-celled  infiltrations  (Aschoff's  bodies)  are  found.  The 
cells  comprising  these  infiltrations  are  probably  derived  from  wandering 
mononuclears  and  not  from  muscle  or  connective  tissue. 

Chronic  Fibrous  Interstitial  Myocarditis.  —  This  is  a  secondary 
productive  process  resulting  in  the  formation  of  fibrous  areas  contain- 
ing elastic  and  connective  tissue.  It  may  follow  acute  myocarditis, 
parietal  endo-myocarditis,  coagulation  necrosis  of  the  cardiac  muscle, 
or  cardiac  abscess. 

Cakdiosclekosis 

Of  late  there  have  appeared  in  the  literature  and  clinical  medicine 
the  generic  terms  cardiosclerosis,  cardiovascular  disease,  and  cardio- 
renal  disease.  These  are  convenient  though  somewhat  inexact  terms 
which  are  meant  to  describe  and  group  certain  clinical  conditions. 
There  is  no  single  pathological  picture  which  accurately  describes 
these  groups.  As  the  names  denote,  the  pathological  change  in  the 
myocardium  and  endocardium  is  an  exceedingly  variable  one.  It 
depends  upon  the  amount  and  type  of  the  other  concomitant  diseases 
affecting  the  kidneys  and  general  arterial  structure.  The  usual  under- 
lying factor  is  a  general  degenerative  change  of  the  entire  vascular 
system,  but  especially  of  the  smaller  arterioles  (the  capillary  fibrosis 
of  Jores)  of  the  heart  and  kidneys.  The  heart  then  presents  changes 
corresponding  to  this  widespread  cause,  in  addition  to  changes  wrought 
by  renal  disease.  The  heart  is  either  atrophic,  with  a  thickened,  sclerosed, 
and  calcareous  endocardium  and  indurated  scars  in  the  myocardium; 
or  it  is  enlarged,  the  coronaries  showing  signs  of  mild  or  widespread 
disease  varying  from  slight  thickening  to  extreme  calcification  and  ob- 
literation of  the  arterial  lumen.  This  process  may  involve  the  smallest 
coronary  branches.  The  aorta  is  dilated,  its  intima  thickened  and 
atheromatous,  containing  calcareous  deposits.  A  similar  process  affects 
the  semilunar  valves  which,  as  a  consequence,  become  incompetent  or 
stenotic.  The  ventricular  endocardium  shows  various  patches  of  fibrotic 
thickening.  Similarly,  the  mitral  valves  are  infiltrated  by  fibrous 
patches  on  their  surface  or  along  their  free  margins.  The  valves  may 
even  be  incrusted  with  calcareous  deposits.  The  myocardium  presents 
indurated  areas  of  scar  tissue  formation,  or  the  entire  musculature  is 
riddled  by  massive  formations  of  this  character.  Engrafted  upon  these 
commoner  changes  are  those  which  frequently  accompany  hypertension 
and  renal  disease,  i.e.  massive  hypertrophy  usually  of  the  left  but 
sometimes  of  both  ventricles. 


CHAPTER  XIII 

CLINICAL   PHENOMENA    AND    SYMPTOMATOLOGY   OF 
ENDOCARDITIS 

For  clinical  purposes,  I  shall  divide  valvular  endocarditis  into  the 
rheumatic,  the  bacterial,  and  the  chronic  streptococcus  viridans.  Car- 
diac syphilis  and  general  cardiosclerosis  are  discussed  separately. 

Rheumatic  Endocarditis 

Clinical  phenomena  accompanying  acute  endocarditis  may  be  di- 
vided into  the  general  rheumatic  and  the  endocarditic  manifestations. 
The  former  include  joint  and  muscular  symptoms,  chorea,  tonsillitis,  ery- 
thema nodosum,  subcutaneous  fibroid  nodules,  etc.  These  rheumatic 
manifestations  do  not  always  run  parallel  with  the  degree  of  endocardial 
involvement :  the  rheumatism  may  be  mild,  the  endocarditis  severe, 
or  the  reverse.  I  have,  for  example,  noted  the  appearance  of  severe 
infection  of  the  mitral  valve  following  very  mild  catarrhal  invasions 
of  the  upper  air  passages.  One  instance  was  that  of  a  young,  vigorous 
adult  of  twenty,  suffering  from  mild  pharyngeal  catarrh.  His  highest 
temperature  was  100.4°.  After  three  days,  a  typical  mitral  lesion  de- 
veloped. 

Endocarditic  manifestations  depend  upon  physical  signs,  and  upon 
the  type,  course,  and  complications  of  the  valvular  infection.  The 
physical  signs  of  the  various  lesions  are  described  in  a  separate  chapter 
(Chapter  X).  Writers  have  classified  endocarditis  according  to  special 
features  (fever,  cerebral  complications,  etc.),  the  assumed  pathological 
process  (verrucous,  warty  and  papillary  endocarditis),  or  the  results 
of  blood  culture.  Since  the  various  groups  merge,  and  bacterial  inva- 
sions (e.g.  streptococcus  viridans)  may  complicate  rheumatic  endocar- 
ditis, sharp  divisions  are  purely  arbitrary  and  cannot  be  maintained.  I 
purpose  therefore  to  describe  the  usual  clinical  type  of  simple  rheumatic 
endocarditis,  with  such  variations  as  are  important. 

The  one  prominent  symptom  of  acute  rheumatic  endocarditis  is 
fever.  When  the  general  rheumatic  manifestations  are  active,  it  may 
be  impossible  to  trace  the  source  of  the  fever,  for  it  may  then  be  due 
to  rheumatism  or  endocarditis.     When  the  rheumatic  course  is  prac- 

165 


166  CLINICAL  CARDIOLOGY 

tically  afebrile,  any  sharp  rise  of  temperature,  especially  if  sustained, 
is  suggestive  of  an  endocardial  involvement.  Fever  continuing  after 
recession  of  rheumatic  signs  in  the  joints  and  elsewhere  is  strongly 
significant  of  endocarditis.  Fever  may  be  so  slight  that  the  tem- 
perature may  have  to  be  taken  frequently  in  order  to  establish  its  pres- 
ence. This  is  especially  true  in  the  mild  type  of  acute  endocarditis 
of  adults.  More  often  there  is  a  rise  of  temperature  of  one  or  two  de- 
grees ;  its  usual  accompaniments  —  lassitude,  anorexia,  and  headache  — 
are  then  present.  Hyperpyrexia  is  uncommon.  An  initial  chill  or 
rigor  is  rare.  It  occasionally  happens  that  there  is  no  rise  of  tem- 
perature during  the  entire  course  of  the  endocarditis ;  this  of  course 
does  not  preclude  the  possibility  of  fever  before  the  patient  came  under 
observation. 

Certain  prodromal  symptoms  suggestive  of  endocarditis  may  exist, 
particularly  in  children,  even  in  the  absence  of  fever.  Such  children, 
otherwise  robust  and  healthy,  complain  of  feeling  tired,  and  become 
anemic  and  less  active.  These  manifestations  have  no  reference  to 
the  heart,  for  the  children  are  not  dyspnoic,  and  physical  signs  of  en- 
docarditis are  not  found.  It  is  only  when  mild  rheumatic  symptoms, 
such  as  fleeting  pains  in  the  limbs,  occur,  that  a  slight  rise  of  temperature 
for  a  few  hours  may  be  observed ;  with  it,  the  physical  signs  of  endo- 
carditis often  become  evident. 

Between  the  very  mild,  almost  non-febrile  cases,  and  the  commoner 
ones  with  moderate  temperature,  there  exist  all  grades  and .  types  of 
febrile  disturbances. 

The  physical  signs  of  acute  endocarditis  are  inconstant;  they 
usually  vary  with  the  intensity  of  the  process.  The  latter  may  be 
slow  and  gradual,  so  that  it  is  only  after  a  long  time  that  frank  physical 
signs  of  valvulitis  appear.  On  the  other  hand,  physical  signs,  especially 
in  children,  may  be  immediate  and  unmistakable.  Once  established, 
the  auscultatory  phenomena  of  the  valvular  affections  are  those  already 
described  (Chapter  X). 

Other  Symptoms  and  Signs  of  Acute  Endocarditis.  —  The  first 
hint  of  endocardial  damage  may  be  slight  acceleration  of  the  pulse. 
In  adults,  the  rate  may  reach  100,  in  children,  120  per  minute.  This 
pulse  acceleration  is  commoner  in  children  than  in  adults.  It  may 
precede  the  physical  signs  of  endocarditis  by  several  days.  This 
occurred  in  a  young  woman  of  twenty-five  with  articular  rheumatism 
and  without  temperature,  who  suddenly  developed  moderate  tachy- 
cardia; several  days  after  rheumatic  manifestations  had  ceased, 
the  physical  signs  of  endocarditis  were  present.  Next  in  frequency  to 
moderate  pulse  acceleration  are  extrasystoles.  Paroxysmal  tachycardia, 
auricular  fibrillation,  and  flutter  are  uncommon.  Prolonged  conduc- 
tion time  is  sometimes  found ;  it  is  regarded  as  an  evidence  of  myo- 
cardial rather  than  of  endocardial  involvement.  In  very  rare  instances 
myocardial  involvement  shows  itself  by  atrio-ventricular  heart  block. 


ENDOCARDITIS  167 

Subjective  symptoms  of  various  kinds  are  sometimes  referred  to 
the  precordium  during  the  course  of  acute  endocarditis.  They  consist 
of  indefinite  sensations  of  weight  or  pressure  on  the  chest.  Occasion- 
ally "  thumping  "  sensations  are  complained  of,  although  the  heart 
rate  is  normal ;  this  seems  due  to  abnormally  strong  ventricular  contrac- 
tions. There  are  at  times  "  sticking  "  or  "  stitch-like  "  precordial  pains 
(Chapter  XXI).  Pain  may  be  present  not  only  over  the  precor- 
dium, but  may  also  radiate  to  the  left  shoulder  and  neck  and  to  the 
left  intercostal  spaces.  In  general,  the  pains  are  not  severe ;  they  are 
more  common  when  tachycardia  is  present. 

Cardiac  decompensation  in  any  of  its  phases  is  very  rare  in  simple 
acute  rheumatic  endocarditis. 

To  summarize :  fever,  anemia,  arrhythmias,  or  precordial  sensations 
constitute  suggestive  signs  of  the  onset  of  acute  rheumatic  endocar- 
ditis. Definite  physical  signs  of  a  valvular  lesion  are  necessary  in 
order  to  clinch  the  diagnosis. 

Exacerbations  of  simple  rheumatic  endocarditis  are,  in  general, 
marked  by  signs  and  symptoms  similar  to  the  original  onset  of  the 
disease.  Rheumatism,  pronounced  or  obscure,  is  often  present.  In 
some  respects,  however,  rheumatic  endocarditic  recrudescences  differ 
from  the  primary  attack.  For  example,  pulse  irregularities  are  more 
frequent.  Tachycardia  —  simple  pulse  acceleration  or  the  paroxysmal 
type  —  is  particularly  common.  Extrasystoles  occur  next  in  frequency. 
Auricular  fibrillation,  present  throughout  the  entire  exacerbation  or 
coming  in  attacks,  is  by  no  means  rare ;  in  this  respect,  especially, 
exacerbations  differ  from  the  original  onset.  Auricular  flutter  is  occa- 
sionally observed.  Subjective  precordial  sensations  are  more  common ; 
they  vary  from  sensations  of  pressure  to  frank  attacks  of  precordial 
distress.  The  physical  signs  of  the  valvular  lesion  are  more  pronounced 
unless  they  are  masked  by  rapid  or  irregular  heart  action.  Mild  dis- 
turbances of  compensation  —  slight  edema  of  the  legs,  enlarged  liver, 
dyspnoea,  etc.,  begin  to  make  their  appearance. 

Chronic  Endocarditis 

Depending  upon  the  duration  and  frequency  of  rheumatic  exacerba- 
tions, the  symptoms  merge  into  those  of  chronic  endocarditis,  the 
group  embracing  the  great  majority  of  cases  of  valvular  heart  disease. 
Patients  with  chronic  endocarditis  and  perfect  compensation  may  con- 
tinue in  good  health  for  years ;  cardiac  symptoms  may  never  occur. 
These  are  the  fortunate  instances  in  which  the  disease  has  become  quies- 
cent and  the  cardiac  damage  has  not  been  extreme. 

The  chief  symptoms  of  chronic  rheumatic  endocarditis  are  due  to 
myocardial  insufficiency  and  to  decompensation.  Brief  reference  must 
here  be  made  to  the  underlying  cardio-muscular  cause  of  decompen- 
sation.    The  heart,  like  voluntary  muscles,  possesses  the  property  of 


168  CLINICAL  CARDIOLOGY 

shortening  during,  and  of  lengthening  after,  contraction.  In  health,  this 
function  is  perfect,  and  permits  without  damage  a  considerable 
degree  of  dilatation  (e.g.  after  exercise).  In  other  words,  it  is  this 
ability  to  contract  and  expand  which  fundamentally  indicates  what  is 
known  as  the  '  cardiac  reserve.'  As  the  result  of  valvular  disease 
there  is  a  varying  amount  of  change  in  the  ventricles  and  their  cham- 
bers ;  this  consists  in  hypertrophy,  dilatation,  and  myocarditis.  These 
abnormal  factors  compromise  to  a  varying  degree  the  underlying 
function  of  lengthening  and  shortening  of  the  cardiac  fibers,  and  hence 
interfere  with  the  reserve  power  of  the  heart.  In  consequence,  the 
cardiac  power  is  decreased,  and  signs  of  decompensation  appear.  There 
is  also  evidence  that  differences  in  tone  may  play  a  part  in  the  symp- 
tomatology. For  example,  patients  may  complain  of  dyspnoea,  of 
vaso-motor  symptoms,  and  even  of  precordial  distress  without  any 
physical  or  clinical  evidence  of  cardiac  dilatation.  These  symptoms 
may  appear  suddenly,  remain  for  a  few  hours  or  a  day,  then  disappear 
without  signs  of  decompensation. 

Dyspnoea.  —  Our  knowledge  of  the  cause  of  dyspnoea  has  been 
advanced  through  recent  chemical  studies  of  the  blood.  Abnormal 
products  or  abnormal  amounts  of  normal  products  producing  so-called 
acidosis  have  been  found.  Experiments  show  that  alkalies  injected 
into  the  blood  stream  cause  apncea,  and  that  very  small  quantities 
of  acids  and  of  acid  salts,  similarly  injected,  produce  hyperpncea. 
Carbon  dioxide  acts  chemically  in  this  respect  like  a  mineral  or  organic 
acid ;  it  causes  an  increase  of  the  hydrogen  ions  in  the  blood,  the 
factor  which  measures  '  acidosis.'  The  respiratory  center  is  quite 
sensitive  to  changes  in  blood  reaction.  The  mechanism  of  its  regula- 
tion is  as  follows :  acidosis  (diminished  blood  alkalinity)  stimulates 
the  respiratory  center  to  increased  activity;  there  is  a  consequent 
reduction  in  carbon  dioxide,  thus  tending  to  keep  the  hydrogen  ion 
concentration  of  the  blood  at  the  normal  level. 

There  are  several  methods  of  estimating  the  carbon  dioxide  content 
of  the  blood.  It  may  be  measured  directly  by  examining  blood  with- 
drawn from  a  vein  (Van  Slyke  method) ;  or  it  may  be  estimated  indirectly 
by  various  apparatuses  for  determining  the  carbon  dioxide  content  and 
tension  of  the  alveolar  air.  The  results  derived  from  these  two  methods 
run  fairly  parallel.  Conclusions  drawn  from  such  examinations  bear 
an  important  relation  to  cardiac  dyspnoea,  as  will  soon  be  shown. 

Cyanosis.  —  It  is  a  common  clinical  observation  that  cyanosis, 
often  a  prominent  sign  in  valvular  disease,  is  not  necessarily  accompanied 
by  marked  dyspnoea.  On  the  other  hand,  patients  of  the  cardio- 
sclerotic  (q.v.)  type,  especially  those  with  renal  complications,  are 
very  apt  to  be  dyspnoic.  They  are  frequently  not  cyanotic;  indeed, 
they  may  be  decidedly  pale.  The  dyspnoea  is  often  nocturnal.  It  is 
thus  evident  that  dyspnoea  is  present  in  two  different  groups  of  cardiac 
patients  :  those  who  are  pale  and  those  with  cyanosis.     In  the  cyanotic 


ENDOCARDITIS  169 

group,  blood  examination  shows  no  abnormal  increase  of  non- volatile 
acids  ;  the  carbon  dioxide  tension  of  the  alveolar  air  is  usually  normal ; 
there  is  no  or  only  slight  decrease  of  blood  alkalinity.  In  the  anemic 
group,  renal  complications  are  frequent,  the  blood  pressure  often  high, 
and  venous  congestion  is,  as  a  rule,  absent ;  the  carbon  dioxide  tension 
of  the  blood  and  of  the  alveolar  air  is  decreased,  the  acid  products 
increased  (acidosis) ;  both  changes  may  be  extremely  marked.  Such 
patients  often  have  uremic  manifestations.  At  present,  the  belief  is 
that  these  abnormal  products  in  the  blood  are  due,  not  to  overproduc- 
tion, but  to  retention  from  renal  insufficiency. 

Cyanosis,  with  no  or  only  slight  dyspnoea,  is  most  strikingly  seen  in 
chronic  uncomplicated  valvular  disease.  Unless  renal  complications 
are  present,  the  tension  of  the  alveolar  air  and  the  blood  alkalinity 
are  within  normal  limits.  The  dyspnoea,  when  present,  is  due  chiefly 
to  venous  engorgement,  the  result  of  myocardial  insufficiency.  This 
venous  stasis  affecting  the  pulmonary  circulation  produces  deficient 
oxygenation,  which  finally  results  in  cyanosis.  Cyanosis  without 
dyspnoea  is  most  often  found  in  chronic,  decompensated  mitral  lesions. 
When  the  patients  are  resting  quietly,  dyspnoea  is  scarcely  evident. 

Visceral  congestion  varies  considerably  in  the  different  valvular 
lesions.  Congestion  of  the  bronchial  system  is  shown,  at  first,  by  symp- 
toms and  physical  signs  of  bronchitis ;  in  the  more  advanced  cases,  by 
pulmonary  congestion  and  hypostatic  pneumonia.  Pleural  transudates, 
especially  right-sided  hydrothorax,  may  be  present ;  this  preference 
for  the  right  side  has  as  yet  not  been  satisfactorily  explained.  The 
liver  may  be  slightly  or  tremendously  enlarged  and  may  even  reach 
the  pelvic  brim.  The  enlargement  may  remain  permanently.  The 
shape  of  the  liver  is  globular,  its  surface  smooth.  With  gradual  conges- 
tion of  this  organ,  there  is  little  or  no  tenderness  on  pressure;  with 
sudden  decompensation  and  consequent  rapid  engorgement,  it  is  tender. 
The  usual  sites  of  tenderness  are  the  epigastrium  and  the  gall-bladder 
region.  At  necropsy  the  spleen  in  chronic  valvular  disease  is  often 
found  enlarged  and  congested.  This  enlargement,  however,  often 
escapes  diagnosis  during  life,  for  the  edge  of  the  organ  is  rarely  pal- 
pable, and  evidence  derived  from  percussion  alone  is  untrustworthy. 

Renal  involvement  ranges  from  moderate  passive  congestion  to 
sclerotic  changes  in  the  glomeruli.  The  former  is  common ;  the  latter 
rare.  Embolic  renal  infarcts  are  also  rare  in  chronic  rheumatic  endo- 
carditis. Renal  congestion  is  shown  by  decrease  in  the  amount  of  urine, 
by  the  presence  of  albumen  and  casts,  and,  in  severe  cases,  by  lessened  ex- 
cretion of  phenolsulphophthalein  (q.v.).  Edema  varies  from  the  mild  form 
found  only  at  the  ankles  to  general  anasarca.  Naturally,  the  latter  is 
usually  observed  in  extreme  cases  of  long-continued  decompensation. 

Precordial  pain  in  chronic  valvular  disease  apparently  depends 
chiefly  upon  the  degree  and  suddenness  of  decompensation.  Its  distri- 
bution and  character  vary  from  a  slight  sensation  of  precordial  heaviness 


170  CLINICAL  CARDIOLOGY 

to  agonizing  attacks  radiating  from  the  chest  to  the  left  shoulder,  left 
scapula,  neck,  abdomen,  and,  rarely,  to  the  legs  (Chapter  XXI). 
Sudden  dyspnoea  and  pain  may  occur  as  the  result  of  a  profound  change 
in  intracardiac  circulation  from  embolus  or  infarct  of  the  coronary  or 
its  branches. 

The  arrhythmias  will  be  discussed  in  connection  with  the  special 
features  of  decompensation  found  in  the  various  valvular  lesions. 

Special  Signs  and  Symptoms  of  Decompensation  in  Chronic 
Rheumatic  Valvular  Lesions 

Decompensated  Mitral  Regurgitation.  —  Venous  stasis  affecting  the 
pulmonary  circulation  is  an  early  symptom ;  hence  bronchitis  is  one 
of  the  first  manifestations  of  heart  failure.  Bronchitis  may  range 
from  a  short,  hacking,  unproductive  cough  to  one  with  numerous  soft, 
mucous  rales  and  areas  of  sibilant  breathing  scattered  over  both  lungs. 
The  latter  complex  accurately  resembles  bronchial  asthma.  Sometimes 
bronchitis  forms  the  predominant  early  feature  of  decompensation. 
Hemoptyses  or  expectoration  of  blood  mixed  with  muco-pus  are  not 
infrequent.  The  patients  are  as  a  rule  cyanotic.  When  cyanosis  is 
extreme,  the  lips  and  extremities  are  bluish,  the  conjunctivae  suffused 
and  discolored.  Even  with  marked  cyanosis,  dyspnoea  may  be  mild 
when  the  patient  is  resting  quietly.  Severe  decompensation  is  accom- 
panied by  the  visceral  congestion  already  described.  The  usual 
subjective  phenomena  are  a  feeling  of  weight  or  pressure  upon  the  chest ; 
severe  precordial  pains  are  rare.  On  the  other  hand,  sensitiveness  to 
pressure  in  the  epigastrium  is  common.  Somnolence  in  the  ex- 
tremely decompensated  cases  with  a  fair  output  of  urine,  is  probably 
due  to  cerebral  congestion  and  edema. 

Moderate  pulse  acceleration  is  the  rule,  extreme  pulse  acceleration 
or  paroxysmal  tachycardia  is  exceptional.  The  usual  cardiac  irregu- 
larities are  extrasystoles  (commonly  ventricular)  and  auricular  fibrilla- 
tion ;  the  extrasystoles  are  observed  in  the  beginning ;  auricular  fibril- 
lation, in  the  later  stages  of  decompensation. 

Decompensated  Mitral  Stenosis.  —  A  subjective  feeling  of  palpita- 
tion combined  with  slight  tachycardia  is  one  of  the  earliest  symptoms. 
It  is  due  not  only  to  moderate  pulse  acceleration,  but  also  to  increased 
violence  of  the  heart  action.  Slight  dyspnoea  accompanies  the  palpita- 
tion. Cyanosis  is  a  comparatively  late  symptom  and  marks  the  period 
of  severe  decompensation.  An  enlarged  and  distinctly  pulsating 
liver  may  be  present  even  when  cardiac  failure  is  not  extreme.  Sharp, 
precordial  "sticking"  pains  are  common;  they  usually  accompany 
the  tachycardia.  Paralysis  of  the  vocal  cord  due  to  paralysis  of  the 
left  recurrent  laryngeal  nerve  occasionally  occurs. 

Ortner  in  1897  first  described  the  connection  between  mitral  stenosis  and 
paralysis  of  the  left  recurrent  nerve.     Since  then,  reports  of  thirty-two  cases 


ENDOCARDITIS  171 

have  been  collected  from  the  literature  by  Cuisset  up  to  1912.     The  various 
theories  held  accountable  for  the  paralysis  may  be  recapitulated  as  follows : 

1.  Ortner's  Theory  :  Recurrent  paralysis  is  due  to  pressure  of  the  enlarged 
left  auricle  upon  the  nerve. 

2.  Kraus'  Theory :  The  right  ventricular  dilatation  present  in  mitral  ste- 
nosis causes  displacement  of  the  heart  to  the  right,  with  consequent  dragging  on 
the  aortic  ligament  and  arch,  and  resultant  stretching  and  paralysis  of  the  nerve. 

3.  Alexander's  Theory :  The  pulmonary  artery,  either  by  its  own  enlarge- 
ment or  indirectly  by  enlargement  of  the  left  auricle,  is  pressed  against  the 
nerve  and  aortic  arch. 

4.  The  nerve  may  be  compressed  and  caught  between  bands  of  pericardial 
and  mediastinal  adhesions. 

All  these  theories  have  had  some  necropsy  support.  Normally,  the  pul- 
monary artery  is  situated  under,  and  divides  immediately  beneath,  the  aortic 
arch ;  below  the  pulmonary  artery  is  the  left  auricle.  It  therefore  seems  im- 
probable that  the  left  auricle,  even  when  extremely  enlarged,  can  exert  sufficient 
direct  pressure  to  produce  recurrent  paralysis,  unless  the  auricle  is  jammed  be- 
tween, or  is  adherent  to,  the  pulmonary  artery  and  aorta.  This  was  the  finding 
in  one  case  that  came  to  necropsy.  In  another  case,  the  left  auricle  was  the 
size  of  a  smaU  fist  and  was  found  pressing  against  the  nerve.  From  careful 
anatomic  studies  of  frozen  sections,  Fetterolf  and  Norris  state  that  the  effect 
of  left  auricular  dilatation  is  pressure  of  the  left  pulmonary  artery  against  the 
aorta,  and  of  the  left  pulmonary  vein  against  the  pulmonary  artery,  thus  forcing 
the  latter  against  the  aorta.  They  believe  that  direct  pressure  alone  of  the 
enlarged  left  auricle  can  scarcely  produce  paralysis  unless  the  auricle  is  squeezed 
between  or  is  adherent  to  the  pulmonary  artery  and  aorta.  They  conclude 
that  anything  which  will  dilate  or  force  upward  the  left  auricle,  the  left  pul- 
monary vein,  or  left  pulmonary  artery  will  tend  to  produce  paralysis,  and  that 
the  latter  must  finally  be  caused  by  the  nerve  being  "  squeezed  between  the  left 
pulmonary  artery  and  aorta  or  aortic  ligament."  This  conclusion  bears  out  the 
common  knowledge  of  the  normal  close  juxtaposition  of  pulmonary  artery  and 
aorta.  A  similar  conclusion  was  reached  by  Frisehauer,  who,  in  a  case  at 
necropsy,  found  the  nerve  compressed  between  the  left  pulmonary  artery  and 
aorta  by  the  pressure  of  the  dilated  left  auricle  and  pulmonary  vein. 

I  had  an  opportunity  of  observing  a  patient  with  mitral  stenosis  in  whom 
there  was  not  only  paralysis  of  the  left  recurrent  nerve,  but  also  a  marked 
difference  in  the  radial  pulses.  The  history  and  the  result  of  the  examination 
in  this  case  was  as  f  oUows  : 

Female,  aged  25,  married  two  years,  with  no  children  or  pregnancies,  had  a 
severe  attack  of  inflammatory  rheumatism  thirteen  years  ago.  There  were  no 
cardiac  symptoms  until  three  years  ago  ;  at  that  time  palpitation  began.  Dur- 
ing the  last  year,  she  has  also  become  somewhat  dyspnceic.  Hoarseness  com- 
menced six  months  ago.  Examination  of  the  larynx  showed  that,  owing  to 
left  recurrent  paralysis,  the  left  vocal  cord  was  immovable  and  somewhat 
shortened,  and  in  the  '  cadaveric'  position.  The  voice  was  indistinct  and 
hoarse.  The  examination  of  the  cardiovascular  system  revealed  the  following : 
There  was  a  noticeable  difference  between  the  right  and  left  radial  arteries  on 
palpation,  particularly  when  the  arms  were  extended  above  the  head.  The 
systolic  and  diastolic  blood  pressures  of  the  right  brachial  were  respectively 
110  and  80  mm.  of  mercury;  of  the  left,  82  and  70  mm.  There  was  no  per- 
ceptible difference  in  the  carotid  pulsations.  The  pulse  was  regular,  the  rate 
100  per  minute.  There  was  vigorous,  visible,  precordial  pulsation ;  a  diastolic 
thrill  was  felt,  and  a  loud,  rumbling,  presystolic  murmur  was  heard,  at  the  apex. 
The  aortic  sounds  were  normal.  Over  the  pulmonary  area  there  was  a  somewhat 
rough  systolic  murmur  and  an  exceedingly  accentuated  snappy  second  sound ; 
the  sharp  click  of  pulmonary  valve  closure  was  also  evident  on  palpation.  A 
dry  pericardial  friction  rub  was  heard  over  the  lower  sternum ;  three  weeks 
later,  there  was  evidence  of  fresh  pericarditis  over  the  pulmonary  area.  There 
was  no  systolic  apical  retraction.  Orthodiascopic  examination  (Fig.  247)  re- 
vealed a  short  aortal  bulge  (A) ;  the  outline  of  the  aorta  was  apparently  en- 
croached upon  by  the  very  much  dilated  pulmonary  artery  (P. A).  The  left 
auricle  (L.A.),  though  not  enlarged  in  the  tracing,  overlapped  the  pulmonary 
artery  to  some  extent.     The  left  ventricle  (L.  V)  and  the  right  side  of  the  heart 


172  CLINICAL   CARDIOLOGY 

were  also  somewhat  dilated.     The  electrocardiogram  showed  a  negative  R  III, 
and  a  notched  and  enlarged  P  in  the  first  lead. 

In  this  case,  there  was  no  evidence  of  abnormal  right  ventricular  enlarge- 
ment ;    the  heart  was  dilated  to  the  left,  as  revealed  by  orthodiascopy.     The 

electrocardiogram  (negative  R  III)  added  some 
corroboration.  This  evidence  of  left  ventricular 
enlargement  tends  to  discredit  Kraus'  theory  as 
to  the  etiology  of  recurrent  paralysis  in  mitral 
stenosis.  The  orthodiascopic  findings  and  physical 
signs  over  the  pulmonary  artery  in  my  case  leads 
to  the  conclusion  that  the  recurrent  nerve  paraly- 
sis was  due  to  dilatation  and  pressure  of  the 
pulmonary  artery  against  the  aorta ;  whether  or 
not  the  left  auricle  was  a  factor  in  pushing  up  the 
pulmonary  artery  it  is  impossible  to  state.  Lian 
and  Marcorelles  insist  on  the  presence  of  old 
thrombosis  of  the  left  auricle,  or  of  a  mediastinitis 
Fig.  247.  —  Orthodiascopic  as  contributory  causes.  Pericarditis  was  present 
tracing:  A,  aortal  outline ;  in  my  patient;  it  was  at  first  confined  to  the 
P. A,  outline  of  pulmonary  precordial  area  over  the  lower  sternum  ;  later,  it 
auricie-  L  F  o  tline  of  involved  tne  area  over  tne  pulmonary  artery. 
fefTven'tricle  '  This  may  have  been  an  added   factor  in  binding 

down  the  dilated  pulmonary  artery. 
A  unique  feature  was  the  presence  of  a  marked  difference  in  the  right  and 
left  brachial  blood  pressures  and  in  the  radial  arteries ;  this,  in  conjunction 
with  paralysis  of  the  vocal  cord,  formed  a  striking  resemblance  to  the  clinical 
syndrome  of  aortic  aneurism.  The  difference  in  brachial  pulse  pressure  seemed 
due  to  the  dilated  pulmonary  artery  being  wedged  under  the  aortal  arch 
opposite  the  origin  of  the  left  subclavian  artery,  with  a  pressure  sufficient  to 
produce  interference  with  the  circulation  of  the  subclavian,  and  consequently 
of  the  left  brachial. 

Attacks  of  paroxysmal  tachycardia  are  frequent  in  decompensated 
mitral  stenosis.  Emboli  produce  occasional  complications.  Hemiplegia 
and  aphasia  may  follow  cerebral  emboli.  As  an  instance,  one  of  my 
patients,  a  woman  aged  50  with  a  mitral  stenotic  lesion,  had  aphasia 
for  10  years  from  a  cerebral  embolus.  A  large  artery  of  the  extremity 
may  be  plugged  by  an  embolus  and  cause  gangrene.  This  happened  in 
a  patient  of  40  with  mitral  stenosis  and  finally  led  to  amputation  of  the 
leg ;  the  patient  recovered. 

Severe  decompensation  in  mitral  stenosis  is  usually  brought  about 
by  the  development  of  auricular  fibrillation,  with  the  usual  signs  and 
symptoms  already  described.  The  arrhythmia,  once  established,  usually 
becomes  permanent.  Occasionally,  however,  fibrillation  occurs  with 
each  fresh  exacerbation  of  endocarditis.  Auricular  fibrillation  is  found 
oftener  in  mitral  stenosis  than  in  any  other  valvular  disease. 

Aortic  Stenosis.  —  The  symptoms  of  heart  failure  depend  chiefly 
upon  the  degree  of  ventricular  hypertrophy  with  its  implied  lowered 
cardiac  efficiency.  Marked  decompensation  is  a  late  symptom,  and  is 
found  only  when  hypertrophy  becomes  extreme.  Congestion  and 
auricular  fibrillation  occur  only  in  the  terminal  stages.  Among  earlier 
symptoms  are  those  due  to  cerebral  anemia  (dizziness  and  faintness). 
Other  beginning  manifestations  consist  of  a  subjective  feeling  of  pal- 
pitation and  of  moderate  tachycardia.  Embolic  infarcts  in  the  viscera 
or  extremities  are  occasional  complications. 


ENDOCARDITIS  173 

Aortic  Regurgitation.  —  The  patients  are  characteristically  prone 
to  suffer  from  attacks  of  tachycardia  (often  paroxysmal),  and  from 
very  severe  precordial  pains.  Pains  and  tachycardia  often  occur 
in  nocturnal  attacks.  The  pains  are  usually  severe,  sometimes  agoniz- 
ing. Their  favorite  site  is  the  precordium ;  they  may  radiate  to  the 
arms,  neck,  abdomen,  and  even  to  the  legs.  Fright,  excitement,  over- 
exertion, or  nervous  strain  may  be  sufficient  to  initiate  an  attack  of 
pain  or  of  tachycardia,  especially  when  ventricular  hypertrophy  is  far 
advanced.  Such  attacks  may  also  represent  the  only  evidence  of  fresh 
endocarditis.  Susceptibility  of  the  heart  to  nerve  influences  of  the  most 
varied  kinds,  a  condition  so  common  in  aortic  regurgitation,  depends 
chiefly,  I  believe,  upon  the  continued  mechanical  insults  from  aortic 
hyperactivity  to  the  branches  of  the  cardiac  plexus  surrounding  the 
root  of  the  aorta.  This  may  well  produce  an  altered  state  of  nerve 
tone  and  of  nerve  control,  leaving  the  heart  readily  susceptible  to 
extraneous  influences. 

Hemoptyses  occasionally  occur  with  the  tachycardial  attacks ; 
they  seem  due  to  acute  pulmonary  congestion  from  rapid  heart  action. 
Hemoptysis  may  also  be  the  result  of  a  pulmonary  infarct.  Another 
occasional  complication  of  aortic  regurgitation  consists  in  periods  of 
somnolence  merging  into  stupor.  In  one  of  my  patients,  a  girl  of  17 
with  a  typical  rheumatic  regurgitant  lesion  and  tremendous  left  ven- 
tricular hypertrophy,  these  cerebral  manifestations  were  usually  ushered 
in  by  fever  up  to  103°,  and  by  paroxysms  of  auricular  fibrillation. 
Cyanosis  was  not  present.  The  dyspnoea  during  these  attacks  was  not 
more  marked  than  usual.  The  fever  and  fibrillation  seemed  due  to 
recrudescence  of  endocarditis.  Meningitis  could  be  excluded.  The 
accompanying  somnolence,  and  later,  stupor,  in  this  and  other  attacks, 
could  scarcely  be  accounted  for  by  the  fever  alone  or  upon  the  sup- 
position of  a  toxemia,  for  the  patient  had  had  a  severe  and  long-con- 
tinued pneumonia  with  higher  fever,  without  any  cerebral  manifestations. 
Perhaps  cerebral  anemia  from  disturbed  circulation  in  the  brain  is  the 
underlying  cause  for  attacks  of  somnolence  and  semistupor  in  patients 
with  well-marked  aortic  regurgitation. 

Visceral  congestion,  edema,  and  permanent  auricular  fibrillation 
represent  late  stages  of  decompensation  in  aortic  regurgitation. 

Therapy  of  Rheumatic   Endocarditis 

In  acute  rheumatic  endocarditis,  or  in  endocarditic  exacerbations 
accompanied  by  general  rheumatic  manifestations,  the  salicylates, 
preferably  salicylate  of  soda,  are  indicated.  Clinical  observation  has 
shown  that  the  salicylates  often  control  general  rheumatic  manifesta- 
tions; it  is  therefore  assumed  that  they  may  control  the  rheumatic 
poison  affecting  the  heart.  I  prefer  to  give  the  salicylate  of  soda  in  15 
grain  doses  hourly  until  tinnitus  occurs,  or  until  six  doses  have  been 


174  CLINICAL   CARDIOLOGY 

taken ;  thereafter,  the  same  dose  should  be  given  three  times  daily. 
The  futility  of  sera  and  vaccines  is  discussed  later  (Chapter  XVI). 
Rest  in  bed  should  be  enjoined  during  the  period  of  the  acute  endo- 
carditic  attack.  The  plan,  sometimes  followed,  of  keeping  patients  in 
bed  many  weeks,  or  even  months,  after  the  acute  stage  has  passed, 
possesses  no  value  in  aiding  the  circulation  or  in  preventing  reinfection 
(Chapter  XVIII).  From  three  to  five  weeks  I  consider  the  average 
time  for  rest  in  bed  after  the  acute  manifestations  have  passed.  In 
those  with  rapid  heart  action  or  with  precordial  discomfort,  an  ice  bag 
should  be  placed  over  the  heart ;  it  should  be  kept  in  a  proper  sling  so 
that  the  patient  is  not  continually  annoyed  by  its  slipping.  The  length 
of  time  that  ice  is  to  be  applied  should  be  governed  to  a  great  extent  by 
the  patient's  feelings.  I  have  occasionally  found  more  relief  from  hot 
applications  (hot  water  bag)  than  from  cold.  If  tachycardia  is  marked, 
or  if  patients  are  restive,  the  bromides  alone,  or  combined  with  small 
doses  of  morphine,  are  indicated.  Occasionally,  hypnotics  (chloral, 
veronal)  are  required.  Digitalis  is  not  indicated,  for  decompensation 
does  not  occur  in  acute  endocarditis.  An  exception  may  be  the  pres- 
ence of  tachycardia  with  acute  dilatation  and  dyspnoea,  a  condition 
more  frequent  in  children  than  in  adults. 

In  chronic  rheumatic  endocarditis,  when  no  decompensation  exists, 
drug  medication  intended  to  affect  the  heart  and  circulation  is  not 
indicated.  Here,  questions  respecting  proper  exercise,  vocation,  and 
occupation  play  important  roles  (Chapter  XVIII).  The  therapeusis  of 
decompensation  in  chronic  endocarditis  is  described,  to  a  great  extent, 
in  another  chapter  (Chapter  XVI).  Though  medication  is,  in  general, 
the  same  for  the  various  valvular  lesions,  it  should  again  be  indicated 
that  the  same  therapy  is  not  followed  by  uniform  results.  The  most 
beneficial  effects  are  derived  from  digitalis  when  employed  in  decom- 
pensated mitral  stenotic  lesions  with  auricular  fibrillation ;  this  follows 
from  the  almost  specific  action  of  digitalis  (q.v.)  upon  the  conduction 
system.  In  the  heart  failure  of  aortic  disease  with  marked  hypertrophy 
digitalis  has  little  or  no  effect  in  relieving  decompensation,  even  in  the 
presence  of  auricular  fibrillation. 

Prognosis 

For  clinical  purposes,  the  question  of  prognosis  in  rheumatic  en- 
docarditis may  be  divided  into  the  acute  and  subacute,  the  quiescent 
and  the  chronic  stages.  The  first  two  are  here  grouped  together 
because  they  overlap  so  frequently  that  a  sharp  distinction  is  impos- 
sible. 

In  the  acute  and  subacute  stages,  the  main  prognostic  problem  is 
to  determine,  if  possible,  the  virulence  of  the  infection.  Although,  as 
stated,  a  few  observers  claim  to  have  isolated  the  specific  organism  from 
the  blood  of  patients  suffering  from  rheumatic  endocarditis,  this  has 


ENDOCARDITIS  175 

not  been  substantiated  by  other  careful  bacteriologists ;  hence,  the 
blood  examination  for  bacteria  cannot  at  present  be  used  to  gauge  the 
severity  of  the  infection.  In  addition  to  information  gained  by  physical 
signs,  most  reliance  regarding  the  degree  of  virulence  in  rheumatic 
valvular  infections  must  be  placed  upon  such  clinical  manifestations  as 
the  acuteness  and  severity  of  onset,  the  frequency  of  chills,  the  presence 
of  hyperpyrexia,  vomiting,  leucocytosis,  severe  anemia,  delirium,  and 
upon  such  complications  as  pericarditis  and  pleurisy  with  effusion.  If 
both  the  aortic  and  mitral  valves  are  affected,  the  acute  and  subacute 
stages  are  apt  to  last  a  longer  time  than  when  one  valve  alone  is  diseased, 
and  the  prognosis  correspondingly  worse.  Patients  with  aortic  lesions 
are  somewhat  more  prone  to  complications  arising  from  the  virulence 
of  the  infection  than  are  those  with  mitral  lesions.  During  the  time 
that  rheumatic  manifestations  are  present,  the  endocarditis  cannot 
be  regarded  as  quiescent,  even  though  there  be  no  clinical  mani- 
festations of  recrudescence.  However,  more  direct  evidence  of  fresh 
endocarditis  may  be  found  in  increased  intensity  and  harshness 
of  endocardial  murmurs,  temporary  arrhythmias,  precordial  "  sticking  " 
pains,  and,  occasionally,  in  embolic  infarcts  in  the  brain,  lungs,  or 
kidneys.  Slight  rises  of  temperature,  if  not  otherwise  accounted  for, 
are  to  be  regarded  as  probable  signs  of  the  continuation  of  the  endo- 
carditic  process.  Another  highly  suggestive  evidence  is  anemia,  severe 
or  moderate,  not  responding  to  the  usual  treatment. 

Occasionally  the  infection  is  mild,  fever  and  other  inflammatory 
manifestations  cease,  the  valvular  lesion  quickly  becomes  quiescent, 
and  indeed  soon  eludes  all  signs  of  ever  having  been  present.  Such 
cases  usually  occur  in  children  and  young  adults,  and  apparently  repre- 
sent instances  in  which  healing  begins  soon  after  the  mild  endocardial 
infection  has  run  its  course.  The  existence  of  such  cases  has  been 
corroborated  by  necropsy  findings. 

If  the  physical  signs  or  clinical  phenomena  indicate  an  active  en- 
docarditis lasting  for  a  month  or  longer,  the  outlook  for  a  "  quiescent  " 
period,  and  therefore  for  a  favorable  prognosis,  becomes  correspondingly 
poor.  These  patients  may  die  of  embolic  infarcts,  or  of  superadded 
bacteremias,  such  as  pneumococcemia  or  streptococcus  viridans  infec- 
tions.    Decompensation  usually  plays  a  minor  role. 

Quiescent  Stage.  —  In  the  fortunate  cases,  this  stage  represents 
uninterrupted  convalescence  from  the  acute  and  subacute,  with 
complete  cessation  of  active  signs  of  endocarditis.  These  patients 
with  their  recurrences  and  exacerbations  comprise  the  great  class  of 
chronic  rheumatic  heart  cases.  Regarding  the  quiescent  stage  as 
convalescence  from  the  acute,  decompensation  is  rare,  the  chances  of 
the  lesion  becoming  '  chronic '  and  remaining  quiescent  are  good.  The 
prognosis  then  depends  upon  that  of  chronic  endocarditis. 

In  chronic  quiescent  cases,  the  cardinal  point  in  prognosis  is  the 
consideration,  not  of  the  number  or  varieties  of  murmurs  present, 


176  CLINICAL   CARDIOLOGY 

but  the  extent  and  type  of  damage  to  the  myocardium,  factors  usually 
decided  by  a  study  of  the  muscular  and  circulatory  efficiency  of  the  heart. 
If  myocardial  efficiency  and  cardiac  reserve  are  good,  a  correspondingly 
good  prognosis  may  be  given.  Regarding  prognosis  from  the  stand- 
point of  longevity,  the  above  observations  must  be  combined  with  a 
general  knowledge  of  the  average  duration  of  life  in  the  various  types 
of  valvular  lesions ;  but  each  case  must  nevertheless  be  studied  in- 
dividually in  the  attempt  to  gauge  the  probable  span  of  life. 

It  has  been  demonstrated  statistically  that  patients  with  mitral 
insufficiency  live  longest ;  individuals  with  this  lesion  living  to  ripe 
old  age  are  not  uncommonly  encountered.  The  usual  duration  of  life 
in  mitral  stenosis  is  much  less ;  one  of  the  reasons  for  this  is  that  such 
cases  are  prone  to  develop  auricular  fibrillation,  and  with  it,  the  usual 
train  of  symptoms  and  dangers  arising  from  decompensation.  In 
aortic  regurgitation,  massive  ventricular  hypertrophies  (cor  bovinum) 
are  common ;  yet  years  may  elapse  until  death  occurs  from  decompensa- 
tion, emboli,  or  from  some  superadded  acute  infective  process.  In 
general,  however,  the  chances  for  longevity  with  this  lesion  correspond 
somewhat  to  the  degree  of  ventricular  hypertrophy;  where  this  is 
marked  or  extreme,  patients  are  not  apt  to  live  beyond  middle  age. 


Acute  Bacterial  Endocarditis 

Other  terms  for  tbjs  affection  are  malignant,  ulcerative,  infectious, 
and  septic  endocarditis.  Bacterial  endocarditis  as  an  acute  process 
engrafted  upon  a  chronic  valvular  lesion  is  not  here  included. 

It  has  already  been  pointed  out  that,  although  not  proven,  rheu- 
matic endocarditis  is  probably  of  bacterial  origin.  But  acute  bacterial 
endocarditis  differs  so  markedly  from  the  rheumatic  type,  and  even 
from  streptococcus  viridans  infection  (itself  a  bacteremia),  that  it  de- 
serves individual  description. 

Acute  bacterial  endocarditis  is  almost  always  a  secondary  process ; 
its  presence  as  a  primary  lesion  has  indeed  been  denied  by  several 
writers.  It  may  complicate  erysipelas,  pneumonia,  puerperal  fever; 
in  fact,  any  bacteremia.  It  is  occasionally  present  as  a  terminal  in- 
fection. Although  the  course  of  acute  bacterial  endocarditis  is  essentially 
acute,  occasional  cases  of  comparatively  long  duration  have  been  de- 
scribed. In  acute  staphylococcic  infections,  the  portal  of  entry  is  the 
skin  or  an  osteomyelitic  focus ;  in  streptococcus  pyogenes,  the  mucous 
membrane  of  the  throat  or  uterus.  Gonococci,  and  also  streptococci 
and  staphylococci,  may  enter  the  general  circulation  from  the  genito- 
urinary tract ;  pneumococci,  from  the  respiratory  tract. 

The  clinical  picture  of  acute  bacterial  endocarditis  is  essentially 
that  of  a  more  or  less  virulent  bacteremia,  with  all  its  protean  and 
manifold   characteristics.     The  disease  rarely  lasts  more  than  four 


ENDOCARDITIS  177 

weeks.  There  are  often  no  cardiac  manifestations ;  no  murmurs,  pain, 
dyspnoea,  or  other  signs  of  cardiac  involvement. 

The  clinical  manifestations  are  sometimes  divided  into  the  typhoid, 
septicemic,  cerebral,  etc.  These  varying  characteristics  depend  upon 
the  virulence  of  the  invading  organism,  and  upon  the  underlying  cause 
of  the  bacteremia  (erysipelas,  puerperal  septicemia,  etc.). 

The  course  of  acute  bacterial  endocarditis  is  usually  marked  by  high 
fever ;  daily  chills  are  common ;  long  remissions  of  temperature  are 
rare.  Sweating  is  often  profuse.  The  onset  of  the  endocarditis  may 
be  marked  only  by  an  intensification  of  the  fever  from  the  original  source 
of  infection,  or  by  an  initial  rigor.  Added  hints  of  its  onset  may  be 
found  in  sudden  increased  pulse  rapidity,  in  sticking  pains  in  the  pre- 
cordium,  in  the  friction  rub  of  dry  pericarditis.  When  the  latter  is 
present,  an  endocardial  involvement  as  well  is  usually  present. 

Septic  infarcts  into  various  organs  mark  the  stormy  progress  of 
the  disease.  Thus,  cerebral  infarcts  may  produce  paralysis' and  uncon- 
sciousness, or,  occasionally,  purulent  meningitis;  symptoms  from  the 
latter  may  then  dominate  the  clinical  picture.  Hematuria,  sometimes 
abundant,  may  follow  a  renal  infarct;  pneumonia,  an  infarct  in  the 
lungs.  Of  frequent  occurrence  are  petechiae.  They  are  usually  nu- 
merous, especially  upon  the  oral  and  conjunctival  mucous  membranes. 
The  petechia?  sometimes  contain  pin-point  pustules  in  the  center. 
Occasionally,  patchy  erythematous  areas  in  the  skin,  resembling  ur- 
ticaria, may  be  found.  Various  joints,  especially  the  larger  ones, 
may  be  involved  in  a  purulent  or  sero-purulent  inflammatory  process. 

The  usual  general  manifestations  of  sepsis,  or  of  a  septic  f  typhoid ' 
condition,  are  common.  The  patients  may  be  actively  delirious,  or 
be  stuporous  and  comatose.  There  may  be  coma  vigil  with  a  dry  and 
coated  tongue. 

Medication,  including  sera  and  vaccines,  possess  no  value.  The 
treatment  is  symptomatic  only. 

Subacute  and  Chronic  Streptococcus  Viridans  Infections 

I  have  made  no  attempt  to  divide  the  disease  into  two  distinct 
stages,  for  the  terms  "  subacute  "  and  "  chronic  "  depend  chiefly 
upon  differences  of  duration  rather  than  of  symptomatology.  The 
usual  duration  is  from  a  month  to  one  year  or  more,  hence  either 
term  may  be  appropriate  to  the  individual  case. 

Pathological  Features.  —  Of  the  chronic  bacterial  infections  of  the 
heart,  that  by  the  streptococcus  viridans  has  been  most  exhaustively 
studied.  The  process  is  almost  always  engrafted  upon  a  chronic  rheu- 
matic infection.  Occasionally,  congenital  lesions  form  the  nidus.  The 
pathological  process  consists  of  vegetative  proliferative  masses  of  gray- 
ish, greenish,  or  pink  color.  Their  main  site  is  the  mitral  valve.  Here 
they  may  form  a  few  soft,  friable  masses,  or  the  valve  may  be  encrusted 


178  CLINICAL  CARDIOLOGY 

with  large  polypoid  lesions.  The  latter  may  then  extend  along  the  left 
auricular  wall  above,  and  the  chorda?  tendina?  below.  The  process  on 
the  chordse  tendinse  occasionally  leads  to  ulceration  and  rupture  of 
these  structures.  Similar  sequela?  are  sometimes  found  as  the  result 
of  vegetations  on  the  mitral.  Proliferative  lesions  on  the  aortic  cusps 
and  walls  are  less  common  and  less  extensive  than  upon  the  mitral. 
Mycotic  aneurisms  of  the  valves  are  occasionally  found. 

Characteristic  changes  in  the  kidney  depend  chiefly  upon  the  presence 
of  infarcts.  When  pyogenic,  they  give  rise  to  numerous  small  congested 
areas  containing  minute  purulent  foci ;  these  are  readily  seen  when  the 
capsule  is  stripped  from  the  kidney.  Non-pyogenic  bland  infarcts 
occasionally  occur ;  they  show  the  changes  usual  to  anemic  necrosis ; 
the  infarcted  areas  are  wedge-shaped  and  may  be  several  centimeters 
in  depth.  When  they  are  recent,  the  cut  surface  is  yellow ;  the  color 
becomes  paler  with  the  process  of  organization.  Another  type  of  in- 
farct, sometimes  assumed  as  pathognomonic  of  chronic  streptococcus 
viridans,  is  embolic  focal  nephritis.  Characteristic  changes  are  then 
found  in  the  glomeruli ;  a  part  of,  or  an  entire  tuft,  may  be  involved. 
The  capillaries  are  congested,  the  glomeruli  contain  a  fibrinous  exudate, 
the  glomerular  epithelium  becomes  swollen,  and  finally  desquamates. 
The  adjacent  parietal  layers  of  Bowman's  capsule  are  often  involved 
in  the  necrotic  process,  so  that  the  entire  necrotic  area  becomes  semilunar 
in  shape.  The  mass  eventually  organizes.  There  is  a  growth  of  epithe- 
lial cells  from  the  healthy  adjacent  Bowman's  capsule,  finally  covering 
the  lateral  surface  of  the  mass.  When  healing  is  completed,  the  result 
is  a  hyaline  area  of  pyramidal  shape. 

The  cerebral  lesions  consist  chiefly  of  areas  of  softening,  following 
emboli.  Occasionally,  cerebral  hemorrhages  from  rupture  of  embolic 
aneurisms  of  the  cerebral  vessels  have  been  observed. 

Clinical  Features.  —  The  pathological  features  enumerated,  and  the 
fact  that  streptococcus  viridans  infection  is  a  bacteremia,  make  it  ap- 
parent that  the  clinical  complex  varies  considerably.  The  predominant 
clinical  features  depend  upon  the  toxemia,  upon  focal  embolic  insults 
in  the  various  organs  and  viscera,  and  upon  the  pronounced  pathological 
changes  in  the  heart  and  kidneys. 

The  onset  of  the  streptococcus  viridans  affection  is  usually  insid- 
ious ;  the  only  complaint  for  days  or  weeks  preceding  the  definite 
febrile  period  may  be  slight  general  malaise  or  mild  anorexia.  Some- 
times the  initial  symptoms  resemble  those  of  other  febrile  invasions : 
rigors,  chills,  vomiting,  and  fever  between  101°  and  103°.  Occasionally 
the  onset  is  even  more  acute,  and  the  daily  temperature  reaches  104° 
or  105°,  with  remissions  resembling  malaria.  Such  initial  symptoms 
usually  betoken  a  stormy  and  comparatively  short  course  for  the  viri- 
dans infection.  When  the  disease  is  once  established,  it  is  usual  to  have 
a  febrile  period  from  one  to  three  weeks,  with  afebrile  intervals  of 
about  the  same  duration.     Each  new  invasion,  at  its  beginning,  may  be 


ENDOCARDITIS  179 

marked  by  severe  chills  and  hyperpyrexia;  temperatures  up  to  106° 
are  occasionally  encountered.  The  disease  may  thus  continue  for 
months  until  emboli  or  exhaustion  produce  death. 

Petechiae  represent  one  of  the  most  prominent  and  frequent  mani- 
festations. They  are  probably  due  to  small  emboli.  On  the  mucous 
membrane,  they  may  appear  as  small,  isolated  red  spots,  with  pale 
centers  surrounded  by  an  area  of  congestion,  and  sharply  defined  from 
the  normal  mucous  membrane.  The  favorite  site  of  petechiae  is  the 
lower  conjunctiva.  Here  they  are  characteristically  found  at  the 
angulation  of  the  vessels ;  the  entire  sac  should  be  well  exposed  by 
pressing  back  the  eyeball.  Occasionally,  petechiae  are  found,  not  in 
the  lower,  but  in  the  upper  lid.  They  are  also  found  upon  various  parts 
of  the  oral  and  even  pharyngeal  mucous  membranes.  In  one  of  my 
patients,  in  whom  petechiae  often  appeared  in  crops  on  the  skin  as 
well  as  on  the  conjunctivae  and  buccal  mucous  membrane,  I  found, 
in  addition,  a  few  in  the  anterior  urethra. 

Skin  petechias  resemble  those  on  the  mucous  membrane.  They 
are  usually  small  and  punctate;  occasionally,  they  become  some- 
what larger.  Very  rarely,  they  are  surmounted  by  minute  pus- 
tules. While  isolated  petechiae  are  the  rule,  it  is  not  unusual  to  have 
them  appear  in  crops  over  various  parts  of  the  body.  Occasionally 
their  appearance  is  attended  by  severe  neuralgic  pains  in  the  area 
corresponding  to  the  location  of  the  rash.  The  cause  of  such  pains  is 
not  apparent.  The  petechiae  are  not  tender;  they  usually  disappear 
within  one  week.  They  sometimes  leave  small  pigmented  spots  for  a  few 
days,  which  must  be  carefully  distinguished  from  other  pigmentations, 
especially  freckles. 

In  addition  to  petechiae,  other  skin  manifestations  are  not  uncommon 
in  this  infection.  Painful  erythematous  nodules,  slightly  red  and  some- 
what tender  (Heubner's  nodes),  may  occur  in  the  terminal  phalanges, 
especially  of  the  fingers.  The  nodules,  usually  multiple,  disappear 
within  a  few  days ;  they  are  probably  of  embolic  origin.  Pyogenic 
emboli  in  the  deeper  dermal  arteries  may  produce  skin  gangrene  or 
necrosis.  This  occurred  in  one  of  my  cases  and  finally  resulted  in 
sloughing  of  the  entire  scrotum.  Emboli  are  sometimes  scattered 
shower-like  through  the  smaller  arteries  of  the  extremities,  producing 
numerous  small  areas  of  deep  or  superficial  gangrene,  and  necrosis  in 
fingers  and  toes.  This  was  well  illustrated  in  a  woman  aged  50  with 
streptococcus  viridans  and  a  decompensated  double  mitral  lesion. 
She  developed  gangrenous  areas  on  several  digits  and  toes,  and  on  the 
dorsum  of  both  hands.     She  died  one  week  later. 

The  hematological  examination  is  of  great  importance.  While  a 
mild  secondary  anemia  with  moderate  leucocytosis  and  a  high  poly- 
nuclear  count  is  the  rule,  anemia  may  become  so  marked  as  to  over- 
shadow the  clinical  picture,  even  leading  to  the  erroneous  diagnosis  of 
non-organic,  instead  of  organic,  endocardial  murmurs.     Occasionally, 


180  CLINICAL  CARDIOLOGY 

the  blood  picture  and  the  hemoglobin  percentage  so  closely  resemble 
pernicious  anemia  that  patients  have  been  treated  for  the  latter  disease ; 
only  at  necropsy  was  the  correct  diagnosis  established. 

Splenic  enlargement  is  quite  common  ;  it  may  vary  from  moderate  in- 
crease in  size  to  one  reaching  several  inches  below  the  free  border  of  the 
ribs.  At  necropsy,  infarcts  of  various  sizes  are  almost  regularly  found 
in  this  organ. 

Changes  in  the  Urine.— A  trace  of  albumen  and  a  few  casts  are 
frequently  found.  More  significant,  when  traced  to  the  kidney  as 
its  source,  is  the  presence  of  a  microscopic  amount  of  blood.  Rarely, 
macroscopic  hematuria  is  present.  The  streptococcus  viridans  can 
only  occasionally  be  cultured  from  a  catheterized  urine  specimen. 
In  exceptional  instances  renal  signs  and  symptoms  predominate  in 
the  clinical  picture.  This  occurred  in  one  of  my  patients.  There 
was  unilateral  renal  colic  and  bleeding.  A  blood  culture  taken  at  that 
time  was  sterile.  A  nephrectomy  was  done ;  the  affected  kidney  was 
found  twice  the  normal  size  and  riddled  with  infarcts.  The  patient 
died  two  weeks  later.  Another  blood  culture,  taken  two  days  before 
death,  was  positive.  At  necropsy,  valvular  lesions  characteristic  of 
steptococcus  viridans  were  found. 

Nervous  manifestations  are  frequent.  They  depend  upon  one  or 
several  factors,  all  of  which  must  be  etiologically  considered.  Stupor, 
for  example,  may  be  due  to  toxemia,  hyperpyrexia,  meningitis,  cerebral 
infarcts,  or  to  uremia.  An  instance  of  the  difficulties  with  which  the 
etiology  of  this  one  symptom  may  be  surrounded  is  that  of  a  woman 
aged  45,  admitted  to  the  hospital  in  semi-stupor.  A  double  mitral 
lesion,  auricular  fibrillation,  and  irregular  fever  were  present.  The 
urine  showed  microscopic  hematuria  and  a  few  renal  elements.  Two 
blood  cultures  were  negative.  A  spinal  tap  was  unsatisfactory.  Semi- 
stupor  finally  merged  into  coma  and  death.  Clinically,  the  symptoms 
seemed  due  to  meningitis.  At  necropsy,  a  double  mitral  lesion,  splenic 
infarct  and  the  glomerular  kidney  changes  of  streptococcus  viridans 
were  found.  Meningitis  was  not  present.  Toxemia  was  the  apparent 
cause  of  stupor  and  coma.  The  most  common  cerebral  lesions  in 
streptococcus  viridans  infections  are  hemiplegias ;  monoplegias  are 
rarer.  Occasionally,  pareses,  not  paralyses,  occur,  to  disappear  during 
the  course  of  the  disease.  Meningitis  is  usually  a  terminal  event; 
its  clinical  signs  may  be  disguised  by  toxic  symptoms. 

Pneumonic  complications  are  not  often  found  in  chronic  streptococcic 
viridans  infections.  Enterorrhagia  from  an  infarct  is  occasionally  met 
with.     Retinal  hemorrhages  sometimes  occur. 

Cardiac  symptoms  (precordial  discomfort,  decompensation,  etc.)  are 
not  regularly  present,  and  then  only  late  in  the  infection.  Even  when 
valvular  vegetations  are  extremely  exuberant,  decompensation  may  not 
occur  during  the  entire  course  of  the  disease.  On  the  other  hand, 
physical  signs  of  a  valvular  lesion  are  usually  frank  and  unmistakable. 


ENDOCARDITIS  181 

This  is  because  of  a  preexisting  valvular  lesion,  and  because  the  strep- 
tococcus viridans  usually  produces  abundant  valvular  vegetations.  Oc- 
casionally, when  the  mural  instead  of  the  valvular  endocardium  is  chiefly 
involved,  murmurs  may  be  faint  and  not  characteristic.  Arrhythmias, 
especially  auricular  fibrillation  and  extrasystoles,  are  not  uncommon. 
When  found  during  the  active  febrile  periods,  they  are  apparently  caused 
by  endocardial,  rather  than  by  myocardial,  involvement,  for  they  usually 
cease  with  the  disappearance  of  fever.  When  present  during  decom- 
pensation, cardiac  irregularities  are  probably  due  to  myocardial  de- 
generation, or  are  indicative  of  myocardial  insufficiency. 

The  study  of  blood  cultures  is  naturally  of  extreme  diagnostic 
importance.  When  properly  made  and  a  sufficient  length  of  time 
(one  week)  is  allowed  for  the  appearance  of  a  growth,  the  organism  has 
been  recovered  in  a  great  majority  of  the  cases.  Sometimes  numerous 
blood  cultures  are  necessary  before  the  organism  can  be  isolated. 

The  clinical  course  of  some  cases  in  which  the  coccus  has  not  been 
recovered  during  life,  and  the  presence  at  necropsy  of  glomerular  lesions 
characteristic  of  streptococcic  viridans  infections,  make  it  probable  that 
some  cases  heal,  or  at  least  remain  quiescent  over  a  long  period  of 
time.  The  quiescent  interval  may  last  several  years.  These  have 
been  grouped  as  being  in  the  "  bacteria  free  stage"  (Libman).  The 
following  cases  are  illustrative  of  this  condition : 

Male,  aged  21,  had  scarlet  fever,  followed  by  severe  endocarditis 
when  7  years  old.  A  double  aortic  and  mitral  regurgitant  lesion  re- 
sulted. For  many  years  there  was  no  decompensation  or  other  symp- 
tom except  occasional  attacks  of  hematuria.  A  few  months  before 
death  the  patient  developed  chills  and  fever ;  the  streptococcus  viridans 
was  then  found  in  the  blood.  In  the  light  of  our  present  knowledge 
this  case  seems  to  belong  to  the  category  just  described.  The  intervals 
between  the  attacks  of  hematuria  probably  represent  long  remissions 
or  "  bacteria-free  stages." 

Male,  aged  40,  entered  the  hospital  with  fever.  He  had  a  mitral 
and  an  aortic  lesion.  Blood  cultures  on  two  occasions  showed  the  strep- 
tococcus viridans.  The  fever  remained  high  for  three  weeks,  during 
which  time  the  patient  was  delirious.  The  temperature  then  gradually 
became  normal.  The  patient  was  not  seen  again  for  one  year.  In 
this  interval  he  said  that  he  had  been  quite  well.  He  was  readmitted 
to  the  hospital  with  a  pneumonia  of  embolic  origin.  The  physical 
signs  of  valvular  disease  were  the  same  as  upon  first  admission.  Blood 
cultures  were  negative.  The  patient  made  a  good  recovery  from  the 
pneumonia. 

The  extent  and  frequency  of  bacterial  reinvasions  (i.e.  the  duration 
of  the  bacteria-free  interval)  are  at  least  partly  governed  by  certain 
characteristics  of  the  vegetations.  If  the  latter  are  covered  by  a  firm, 
partially  organized  fibrin  layer,  the  bacteria  are  not  as  apt  to  invade 
the  blood  stream ;  while  if  the  fibrin  layer  is  thin  or  is  so  situated  that 


182  CLINICAL   CARDIOLOGY 

the  blood  stream  impinges  with  full  force  against  it,  the  bacteria  are 
much  more  likely  to  be  washed  into  the  blood  current.  The  amount  of 
fibrin  covering  the  vegetations  probably  depends  upon  the  virulence 
and  proteolytic  digestive  power  of  the  invading  organism. 

Besides  symptomatic  treatment,  therapy  consists  in  the  use  of 
vaccines,  preferably  autogenous,  and  of  horse  serum  sensitized  to 
various  strains  of  the  streptococcus  viridans.  An  occasional  cure  by 
these  methods  has  been  reported.  In  view  of  the  exceptionally  long 
remissions,  sometimes  for  years  without  the  use  of  vaccines,  final  judg- 
ment regarding  "  cures  "  by  serum  or  vaccine  treatment  should  for  the 
present  be  withheld.  In  my  own  cases  I  have  observed  no  effect  upon 
the  course  of  the  disease  from  serum  or  vaccine  therapy ;  nor  was  there 
any  evident  arrest  of  the  pathological  process.  This  was  shown  by  the 
examination  of  such  hearts  at  necropsy.  For  example,  in  one  case  in 
whom  the  diagnosis  of  streptococcus  viridans  infection  was  established 
by  blood  culture  four  days  after  the  initial  chill,  not  only  did  autogenous 
vaccines  and  sensitized  horse  serum  administered  for  months  have  no 
effect  upon  the  symptoms  or  course  of  the  disease,  but  the  post-mortem 
examination  showed  exuberant  and  fresh  masses  of  vegetation  literally 
plastering  the  mitral  valves,  the  left  ventricle,  and  auricle.  Unfor- 
tunately, therapy  of  all  kinds,  including  intravenous  injections  of  silver 
salts  (Chapter  XVI),  must  at  this  time  be  regarded  either  as  futile  or 
as  purely  in  the  experimental  stage.  The  wisdom  of  prophylactic 
vaccination  against  viridans  infection  in  those  cases  in  whom  its  later 
occurrence  is  feared  deserves  careful  consideration. 

REFERENCES 

Chapters  XI-XIII 

Adler,  I. :   Syphilis  of  the  Heart,  1898. 

Adler,  I.,  and  Hensel,  O. :   Intravenous  Injections  of  Nicotine  and  their  Effects 

upon  the  Aorta  of  Rabbits ;  Journal  of  Medical  Research,  N.S.,  X,  229. 
Asehoff,  L. :   Pathologische  Anatomie,  II  Edition,  I,  32. 
Baehr,  G. :  Glomerular  Lesions  of  Subacute  Bacterial  Endocarditis ;  Journal  of 

Experimental  Medicine,  1912,  XV,  330. 
Brooks,  H. :    The  Heart  in  Syphilis;    New  York  State  Journal  of   Medicine, 

1916,  XVI,  185. 
Brooks,  H. :  The  Tobacco  Heart ;  New  York  Medical  Journal,  1915,  CI,  830. 
Cushny,  A.  R. :  Pharmacology  and  Therapeutics,  7th  Edition,  1914. 
Delafield,  F.,  and  Prudden,  T.  M. :  Text  Book  of  Pathology,  9th  Edition. 
Fleming,  G.  B.,  and  Kennedy,  A.  M. :  A  Case  of  Complete  Heart  Block  in  Diph- 
theria with  an  Account  of  Post-mortem  Findings  ;  Heart,  1910-1911,  II,  77. 
Gy,  A. :    L' Intoxication  Tabagique  chez  l'Homme ;   Paris  Theses,   1908-1909, 

203. 
Hartzell,  T. :    The  Clinical  Type  of  Arthritis  Originating  about  the  Teeth ; 

Journal  of  American  Medical  Association,  1915,  LXV,  1903. 
Hecht,   A.  F. :    Der  Mechanismus    der   Herzaction   im   Kindesalter ;     Ergeb- 

nisse  der  Innere  Medizin  und  Kindesheilkunde,  1913,  XI. 
Heiberg,   H. :    Ein  Fall  von   Endocarditis  Ulzerosa,   etc. ;    Virchow's  Archiv 

fuer  Pathologische  Anatomie  und  Physiologie,  1872,  LVI,  407. 
Horder,  T.  J. :  Infectious  Endocarditis  ;   Quarterly  Journal  of  Medicine,   1908- 

1909,  II,  289. 


ENDOCARDITIS  183 

Hume,  W.  E.,  and  Clegg,  S.  J. :  A  Clinical  and  Pathological  Study  of  the  Heart 
in  Diphtheria  ;   Quarterly  Journal  of  Medicine,  1914-1915,  VIII. 

Jamin,  F.,  und  Merkel,   H.  :    Die  Coronararterien  des  menschlichen  Herzens 
1907. 

Jochmann  :    Ueber  Endocarditis  Septica ;    Berliner  Klinischer  Woehenschrift 
1912,  XLIX,  I,  436. 

Jores,  L. :  Wesen  und  Entwickelung  der  Arteriosklerose  ;   Wiesbaden,  1903. 

von  Juergensen,  T. :  Endocarditis  ;  Nothnagel's  Encyclopedia  —  American  Edi- 
tion, 1908. 

Kaufman,  E. :  Lehrbuch  der  speziellen  pathologischen  Anatomie  ;  Edition  1907. 

Krehl,  L.  :    Ueber  fettige  Degeneration  des  Herzens ;    Deutsehes  Archiv  fuer 
Klinische  Medizin  ;   LI,  416. 

Langly,  J.  N.,  and  Sherrington,  C.  S.  :  Journal  of  Physiology,  1891,  XII. 

Libman,  E. :    A  Study  of  the  Endocardial  Lesions  of  Subacute  Bacterial  En- 
docarditis, etc. ;  American  Journal  of  Medical  Sciences,  1912,  CXLIV,  313. 

Litten,  M. :   Die  Endocarditis  und  ihre  Beziehungen  zu  anderen  Krankheiten ; 
Verhandlungen  d.  Kongresses  fuer  Innere  Medizin,    1900,  XVIII,  97. 

Lucien   et    Parisot :     Quoted   by  Vaquez ;     Archives    des  Maladies  de  Cceur, 
1915,  VIII,  678. 

Neuhof ,  S. :   Functional  Heart  Block  in  Pneumonia ;   Journal  of  the  American 
Medical  Association,  1914,  LXIII,  577. 

Newburg,  L.  H.,  and  Porter,  W.  T. :   The  Heart  Muscle  in  Pneumonia  ;  Journal 
of  Experimental  Medicine,  1915,  XXII,  123. 

Osier,  W.,  and  McCrae,  T. :  System  of  Medicine,  IV. 

Poyton  and  Paine  :   Researches  on  Rheumatism. 

RoMtansky,  von  C. :  Lehrbuch  der  Pathologischen  Anatomie,  II  Edition,  1861. 

Romberg,   E. :    Ueber  die  Erkrankungen  des   Herzmuskels  bei  Typhus   und 
Scharlach ;    Deutsehes  Archiv  fuer  Klinische  Medizin,  1891,  XLVIII,  369. 

Rosenau,   E.   C. :  Elective  Localization  of  Streptococci ;  Journal  of  American 
Medical  Association,  1915,  LXV,  1687. 

Stein,  R. :  Angina  Pectoris ;  Medical  Record,  1915,  LXXXVIII,  131. 

Thorel,  C. :  Ergebnisse  der  Allgemeine  Pathologie  ;   1904,  IX,  Part  I,  559. 

Warthin,  A.  S. :   Transactions  of  the  Association  of  American  Physicians,  May 
15,  1914. 


CHAPTER  XIV 
CARDIAC   SYPHILIS 

As  a  rare- complication  in  the  secondary  stage  of  syphilis,  it  has 
been  found,  pathologically,  that  the  myocardium  alone  may  be  occa- 
sionally involved.  Such  involvements  may  be  sufficient  to  produce 
symptoms  of  myocardial  insufficiency :  dyspnoea  on  exertion,  in- 
definite precordial  distress  and  pain,  precordial  sensitiveness  to  pres- 
sure, slight  pretibial  edema,  sometimes  also  a  faint  systolic  murmur 
at  the  apex. 

The  symptoms  of  cases  in  the  tertiary  stage  depend  upon  the  degree, 
extent,  and  admixture  of  muscular,  valvular,  and  endocardial  involve- 
ment. 

In  occasional  cases,  isolated  luetic  valvulitis  of  the  mitral  or  tricuspid 
has  been  found.  In  a  vast  majority  of  instances,  however,  the  aortic 
valves  bear  the  brunt  of  the  endocardial  infection.  In  addition  to  the 
cusps,  there  is  often  widespread  destruction  of  the  aortic  walls,  finally 
resulting  in  aneurismal  dilatations  (q.v.)  and  in  true  aneurisms.  Ac- 
companying the  aortitis  are  changes  affecting  the  myocardium,  the  re- 
mainder of  the  endocardium,  and  the  coronaries.  Together,  they  com- 
prise a  composite  picture  often  similar  to  that  found  in  non-luetic 
cardiosclerosis  (Chapter  XII). 

In  the  absence  of  a  history  of  venereal  infection  or  of  other  signs  of 
syphilis,  the  presence  of  a  strongly  positive  Wassermann  blood  reac- 
tion is  of  paramount  importance  in  the  diagnosis  of  cardiovascular 
syphilis.  More  than  one  blood  examination  may  be  necessary,  or 
provocative  injections  of  mercury,  or  small  doses  of  salvarsan  may  be 
required  in  order  to  obtain  a  positive  Wassermann  reaction.  If  the 
blood  Wassermann  remains  negative,  the  chemical  and  cytological 
examination  of  the  spinal  fluid  may  indicate  the  presence  of  syphilis. 
Thus  tested  by  routine  and  other  methods,  the  diagnosis  of  cardiovas- 
cular syphilis  can  be  substantiated  in  the  great  majority  of  suspected 
cases. 

From  the  clinical  standpoint,  the  characteristic  symptomatology  and 
signs  of  tertiary  cardiac  syphilis  depend  mainly  upon  the  presence  of 
aortitis  alone,  or  upon  it  as  part  of  the  picture  of  cardiosclerosis.     In 

184 


CARDIAC   SYPHILIS  185 

the  exceptional  instances  in  which  the  myocardium  alone  is  affected, 
the  diagnosis  rests  upon  the  usual  manifestations  of  severe  myocarditis. 
The  possibility  of  gummata  in  the  myocardium  must  also  be  considered. 
They  add  to  the  probability  of  the  occurrence  of  a  myomalaceous  focus, 
or,  when  involving  the  conduction  system,  upon  the  presence  of  heart 
block. 

Aneukismal  Dilatations  of  the  Aorta 

A  century  ago  Hodgson  made  the  fundamental  distinction  between 
sacculated  and  "  dilatation  aneurisms."  He  defined  the  latter  as  a 
"  preternatural  permanent  enlargement  of  the  cavity  of  an  artery." 
The  former  is  a  definite  protrusion  of  only  one  side  of  its  wall  and  may 
include  a  small  or  large  part  of  the  arterial  caliber.  This  distinction 
is  of  clinical  importance  in  aortic  disease.  The  French  still  apply  the 
term  "  Maladie  de  Hodgson  "  to  aneurismal  dilatations  of  the  aorta 
associated  with  valvular  insufficiency.  Aortitis  of  the  ascending  and 
transverse  aorta  is  now  known  to  be  of  luetic  origin  in  the  great 
majority  of  instances.  The  pathology  and  mechanism  of  aneuris- 
mal dilatations  of  these  parts  of  the  aorta  have  been  described  in  detail 
by  Thoma,  who  had  studied  ninety-two  cases.  He  ascribes  their  fun- 
damental cause  to  lessened  resistance  of  the  arterial  walls,  and  categor- 
ically states  that  "  such  weakened  condition  is  not  found  in  the  descend- 
ing thoracic  aorta,"  which  showed  no  change  macroscopically.  The 
pathological  process  in  dilatations  of  the  first  and  second  parts  of  the 
aorta  consists  of  a  mesaortitis,  with  perivascular  infiltrations  of  the 
vasa-vasorum,  small-celled  or  granulomatous  infiltration  in  areas  of 
the  media,  and  splitting  and  destruction  of  the  muscular  and  elastic 
tissue  layers.  Diffuse  dilatation  of  the  entire  thoracic  aorta  from  its 
root  to  the  diaphragm  is  occasionally  seen.  I  have  observed  three 
such  cases  :  one  was  an  autopsy  finding  and  included  severe  myocarditis 
and  coronary  sclerosis,  the  other  two  were  diagnosed  by  physical  signs 
in  conjunction  with  fluoroscopy. 

The  orthodiascopic  picture  of  dilatation  of  the  first  portion  and  arch 
of  the  aorta  has  already  been  described  (Chapter  IX).  On  auscultation 
the  normal  first  sound  at  the  right  base  is  accompanied  or  replaced  by 
a  soft  blowing  murmur,  usually  not  transmitted  beyond  the  first  and 
second  right  interspaces.  Occasionally  the  first  sound  is  faint  or  absent. 
The  second  sound  is  accentuated,  of  varying  quality,  and  is  best  de- 
scribed as  bell-like,  metallic,  or  tinny ;  it  is  often  followed  by  a  soft 
diastolic  murmur,  indicative  of  aortic  insufficiency.  The  accentuated 
and  metallic  quality  of  the  second  sound  is  not  always  due  to  extreme 
hypertension,  for  it  is  frequently  present  with  normal  or  very  slightly 
raised  systolic  blood  pressure.  The  factor  most  responsible  for  this 
abnormal  second  sound  is,  I  believe,  the  aortic  dilatation  acting  acous- 
tically as  a  sounding  box  in  reflecting  and  thus  changing  the  character 
of  the  sound. 


186  CLINICAL  CARDIOLOGY 

In  marked  aneurismal  dilatation,  especially  of  the  arch  of  the  aorta, 
there  is  often  visible  aortic  pulsation  in  the  jugulum.  When  not  visible, 
it  may  be  felt  by  insinuating  the  finger  behind  the  manubrium  sterni. 
In  cases  of  aneurismal  dilatation  of  the  first  part  of  the  aorta,  there  may 
be  more  marked  right  than  left  carotid  pulsation,  a  fact  determined  by 
placing  the  finger  deeply  behind  the  respective  clavicles.  At  the  apex, 
there  is  frequently  a  soft  systolic  murmur,  probably  due  to  relative 
mitral  insufficiency,  or  there  may  be  a  loud  murmur  due  to  thickening 
of  the  mitral  cusps  and  mural  endocardium.  If  the  aneurismal  dilata- 
tion is  accompanied  by  left  ventricular  hypertrophy  and  by  hyperten- 
sion, there  may  also  be  a  reduplicated  apical  impulse  or  a  somewhat 
accentuated  first  sound  at  the  apex,  as  well  as  a  slightly  metallic  second 
sound. 

Reports  of  aortitis  are  almost  entirely  confined  to  disease  of  the 
ascending  or  transverse  aorta  with  fragmentary  or  no  reference  to  the 
descending  thoracic.  McCrae,  Allbutt,  Osier,  and  others  consider 
aneurismal  dilatation  of  the  descending  thoracic  aorta  extremely  in- 
frequent, a  statement  apparently  based  upon  post-mortem  findings,  for 
no  symptomatology  is  mentioned  nor  had  a  clinical  diagnosis  been 
made.  My  object  is  to  indicate  through  illustrative  cases  the  com- 
parative frequency,  diagnosis,  symptomatology,  and  therapy  of  aneu- 
rismal dilatations  of  the  descending  thoracic  aorta  and  to  present  its 
claim  to  a  clinical  entity. 

Male,  age  sixty-seven,  had  never  been  seriously  ill  previous  to  his 
present  complaint.  He  had  been  a  heavy  smoker  and  had  suffered  from 
a  venereal  infection  forty  years  ago,  for  which  he  had  received  many 
subcutaneous  injections  (presumably  of  mercury).  His  present  illness 
began  two  years  ago  with  exceedingly  mild  symptoms :  very  slight  pre- 
cordial pains  when  lying  on  the  left  side,  and  slight  dyspnoea  upon 
climbing  stairs.  Upon  examination,  the  patient  looked  well  preserved, 
the  carotid  pulsation  on  both  sides  was  somewhat  exaggerated,  there 
was  a  belt  of  small  dilated  capillaries  over  the  lower  part  of  the  chest. 
The  cardiac  thrust  at  the  apex  and  the  systolic  impact  at  the  right  base 
were  somewhat  exaggerated.  The  cardiac  area  seemed  normal  to  per- 
cussion. At  the  base  there  was  a  double  murmur,  a  rough  systolic  and 
a  softer  diastolic,  transmitted  and  best  heard  to  the  left  of  the  middle 
third  of  the  sternum ;  a  definite  sensation  of  heaving  impulse  was  im- 
parted to  the  examining  hand  placed  over  the  same  area.  Similar  but 
fainter  murmurs  were  heard  at  the  apex.  Both  radial  pulses  were  alike  : 
the  average  systolic  blood  pressure  was  170  mm.,  the  diastolic,  70. 
Neurological  and  other  examination  revealed  no  abnormalities.  There 
was  slight  pretibial  edema.  The  Wassermann  reaction  was  negative. 
The  roentgenogram  (Fig.  233/  Plate  XIX)  and  orthodiascope  tracing 
(Fig.  232)  showed  a  long  fusiform  dilatation  of  the  entire  descend- 
ing thoracic  aorta.  The  electrocardiogram  presented  evidence  of  left 
ventricular  preponderance,  i.e.  negative  R  III.     Treatment  consisted 


CARDIAC   SYPHILIS  187 

of  one  salvarsan  and  many  mercurial  injections ;  iodide  of  potash  in 
moderate  doses  was  administered  in  alternate  periods  of  two  weeks. 
Tincture  of  digitalis  was  given  for  one  week  until  the  edema  of  the 
legs  disappeared.  The  patient  has  been  under  observation  for  several 
years  ;  he  has  been  quite  comfortable,  with  no  pains  for  more  than  one 
year ;  the  physical  signs  along  the  middle  third  of  the  sternum  have 
markedly  receded. 

Female,  age  forty-seven  years,  married  sixteen  years,  had  never 
been  pregnant.  Prior  to  the  present  illness  she  complained  of  dyspnoea 
on  exertion,  and  of  nocturnal  palpitation  accompanied  by  pain  in  the 
lower  precordium.  She  lost  about  forty  pounds  since  her  illness  began. 
One  week  before  admission  to  the  hospital  her  legs  became  edematous. 
The  patient  was  emaciated,  the  right  pupil  was  somewhat  larger  than 
the  left,  both  reacted  sluggishly  to  light  but  normally  in  accommoda- 
tion ;  the  knee  reflexes  were  diminished ;  Romberg's  sign  was  absent. 
The  patient  was  dyspnceic  even  when  at  rest.  There  was  vigorous, 
visible  carotid  and  jugular  pulsation ;  the  aortic  thrust  could  be  plainly 
felt  by  pressing  the  finger  tip  behind  the  manubrium.  By  placing  the 
eye  on  a  level  with  the  patient's  chest,  two  distinct  areas  of  impact  were 
discernible ;  one  corresponding  to  the  apical  region,  the  other  to  an 
area  slightly  to  the  left  of  the  lower  half  of  the  sternum.  The  latter 
impact  was  also  palpable  by  sinking  the  fingers  in  the  lower  left  inter- 
costal spaces,  and  also  by  auscultating  with  the  stethoscope  over  this 
area  in  the  routine  manner.  There  was  no  precordial  tenderness.  The 
apex  was  felt  most  distinctly  in  the  sixth  interspace,  a  considerable 
distance  (14  cm.)  from  the  midsternal  line.  Over  the  base,  and  par- 
ticularly to  the  left  of  the  midsternum,  there  was  a  rough  systolic  mur- 
mur and  a  somewhat  accentuated  second  sound  merging  into  a  soft 
murmur  occupying  the  entire  diastole.  Friction  sounds  indicative  of 
dry  pericarditis  were  present  at  the  base  and  apex.  There  was  slight 
edema  of  the  legs.  The  Wassermann  reaction  was  negative  upon  first 
examination ;  some  months  later  it  became  positive.  The  systolic  blood 
pressure  ranged  between  200  and  180  mm.,  the  diastolic  between  100 
and  40  mm. ;  the  pressure  in  both  arteries  was  equal.  The  urine  was 
normal.  The  roentgenogram  (Fig.  234,  Plate  XX)  showed  fusiform 
aneurismal  dilatation  of  the  entire  descending  thoracic  aorta ;  ortho- 
diascopic  examination  corroborated  this  finding.  The  electrocardiogram 
presented  evidence  of  left  ventricular  preponderance.  The  patient 
refused  treatment ;  she  has  since  reentered  the  hospital,  with  signs  of 
severe  cardiac  failure.  She  subsequently  received  iodide  of  potash 
and  mercurial  injections,  with  marked  improvement. 

Male,  age  fifty-three  years,  laborer,  married.  Venereal  infection 
denied.  Three  and  one  half  years  ago  substernal  pains  and  dyspnoea 
upon  walking  appeared.  One  year  ago  he  was  compelled  to  stop  work 
because  of  the  frequency  and  severity  of  these  attacks.  The  pains 
usually  radiated  to  both  sides  of  the  chest,  the  shoulders,  and  right  side 


188  CLINICAL   CARDIOLOGY 

of  the  head.  During  the  last  few  months  he  had  frequent  pharyngeal 
spasms  upon  attempting  to  swallow  fluids,  so  that  there  was  occasional 
regurgitation  through  the  nose.  There  were  no  gastric  symptoms. 
The  patient  looked  florid  and  well  nourished ;  there  was  no  dyspncea 
when  at  rest.  Upon  admission  to  the  hospital  the  right  radial  pulse 
was  much  smaller  than  the  left ;  there  were  no  abnormal  carotid  or  jugular 
pulsations.  The  apex  beat  was  best  heard  in  the  fifth  interspace,  7 
cm.  from  the  midsternal  line.  On  auscultation  the  first  sound  at  the 
apex  was  scarcely  audible ;  the  second  was  normal.  The  first  sound  at 
the  right  base  could  not  be  heard ;  the  second  aortic  was  normal.  Both 
were  distinctly  heard  to  the  left  of  the  middle  third  of  the  sternum,  the 
first  sound  there  being  normal  in  intensity,  the  second  somewhat  ac- 
centuated. There  was  no  edema  of  the  legs.  Examination  of  the 
other  organs  revealed  nothing  abnormal.  The  Wassermann  test  was 
negative.  An  interesting  phenomenon  was  the  fact  that  intermittently 
for  several  weeks  the  right  radial  was  smaller  than  the  left,  the  differ- 
ence sometimes  amounting  to  40  mm.  of  mercury  in  the  systolic  brachial 
pressures.  These  inequalities  had  no  relation  to  the  symptoms.  The 
roentgenogram  showed  a  distinct,  somewhat  tubular  shadow  behind  the 
hypertrophied  left  ventricle.  With  the  orthodiascope  the  shadow  of 
the  dilated  descending  aorta  could  be  faintly  seen  through  the  upper 
ventricular  shadow.  The  electrocardiogram  presented  the  usual  evidence 
of  left  ventricular  preponderance.  The  patient  was  given  three  in- 
jections of  salvarsan  intravenously,  and  numerous  mercurial  injections 
in  combination  with  iodide  of  potash.  The  pains  and  pharyngeal  spasms 
gradually  subsided;  the  pulse  inequalities  became  only  occasionally 
noticeable  and  finally  disappeared.  The  abnormal  physical  signs  to 
the  left  of  the  sternum  markedly  receded.  The  patient  returned  to 
work ;  his  present  complaint  consists  in  slight  occasional  substernal  pain 
on  walking. 

Male,  age  thirty-eight  years,  a  vigorous  and  healthy-looking  man, 
complained  during  the  last  six  months  of  slight  dyspnoea  upon  climbing 
stairs,  but  none  when  at  rest.  He  was  a  heavy  cigar  smoker.  He  had 
gonorrhea  twenty  years  ago  and  denied  any  other  illness.  The  blood 
pressure  was  normal.  There  was  vigorous  carotid  pulsation  at  the  root 
of  the  neck.  There  was  no  pain  on  precordial  pressure.  The  apex  beat 
was  strong,  and  was  felt  most  plainly  in  the  fourth  interspace,  11  cm. 
from  the  midsternal  line.  A  soft  systolic  murmur  was  heard  at  the  apex. 
At  the  base  the  first  sound  was  impure,  the  second  not  accentuated  but 
prolonged  and  somewhat  liquid  in  character  occupying  the  entire 
diastole.  These  abnormal  sounds  were  heard  loudest  and  most  dis- 
tinctly along  the  middle  left  sternal  border.  The  eye  placed  on  the 
level  with  the  chest  could  discern  a  slight  systolic  heave  over  the  latter 
area,  apparently  distinct  from  that  at  the  apex.  The  other  organs  were 
normal.  The  Wassermann  reaction  was  negative.  The  roentgeno- 
gram showed  dilatation  of  the  upper  part  of  the  thoracic  aorta,  the  latter 


CARDIAC   SYPHILIS  189 

being  visible  as  a  somewhat  denser  shadow  behind  the  ventricles.  The 
orthodiascope  confirmed  this.  The  electrocardiogram  was  normal. 
The  patient  was  given  salvarsan,  .3  gm.  intravenously,  and  many  bi- 
chloride injections  combined  with  iodide  of  potash.  The  dyspnoea  has 
entirely  disappeared  ;  the  abnormal  sounds  at  the  base  and  left  sternum 
are  much  less  pronounced  than  at  the  first  examination. 

Male,  age  fifty-three,  entered  the  hospital  in  the  surgical  service  of 
a  colleague  and  did  not  come  under  the  writer's  observation.  The  his- 
tory was  that  of  an  esophageal  stricture  situated  in  the  mid-thoracic 
region.  The  aneurismal  dilatation  was  discovered  in  making  a  routine 
roentgenographic  examination  of  the  chest.  The  stricture  was  pre- 
sumed to  be  due  to  compression  by  the  dilated  aorta.  The  Wasser- 
mann  test  was  not  done.  The  patient  passed  from  observation.  The 
case  is  included  here  because  the  roentgenogram  is  typical  of  aneurismal 
dilatation  of  the  descending  aorta. 

Symptomatology.  —  Sharp,  continuous,  gnawing  pains,  such  as  those 
often  associated  with  sacculated  aneurism,  are  not  prominent  features 
of  dilatation  of  the  descending  aorta.  When  present,  substernal  pains 
or  those  referred  to  different  parts  of  the  chest,  neck,  or  head  are  most 
apt  to  occur  with  exercise.  It  is  difficult  to  state  the  exact  etiology  of 
these  pains.  They  are  probably  not  due  to  pressure  of  the  dilated  aorta 
upon  the  surrounding  structures  (esophagus,  ribs,  dorsal  vertebra,  inter- 
costal nerves,  etc.).  In  one  case  pain  may  have  been  due  to  esophageal 
stricture  rather  than  to  aortal  pressure.  In  general,  the  elongated  con- 
tour of  the  aneurismal  dilatation  would  in  itself  argue  against  pressure 
upon,  or  erosion  of,  surrounding  tissues.  The  rich  nerve  and  ganglionic 
plexus  surrounding  the  root  of  the  aorta,  and  the  nerve  fibers  and  iso- 
lated nerve  cells  which  have  been  described  in  the  connective  tissue 
of  its  middle  coat,  may  explain  how  various  grades  of  inflammation  in 
the  aorta  and  how  differences  of  aortal  pressure  and  dilatation  can  give 
rise  to  these  referred  pains.  In  addition,  periaortitic  inflammation  with 
possible  involvement  of  the  neighboring  nerve  structures  can  also  cause 
neuralgic  symptoms.  Similar  nerve  involvement  has  been  found  in 
dilatations  of  the  ascending  aorta  and  arch.  The  assumption  of  inflam- 
matory exacerbations  within  or  without  the  aorta  is  corroborated  by 
the  occasional  rapid  subsidence  of  the  pains  following  salvarsan  in- 
jections. This  result  is  probably  ascribable  to  control  of  these  exacer- 
bations, although  Vaquez  and  Laubry,  and  Vaquez  and  Bordet  claim 
that  there  is  sometimes  a  reduction  in  the  size  of  sacculated  aneurisms 
after  several  salvarsan  injections.  The  writer  has  not  been  able  to 
determine  any  difference  in  the  size  of  the  dilated  descending  aorta  as 
the  result  of  therapy.  In  addition  to  the  aortal  disease  it  must  be 
remembered  that  accompanying  coronary  sclerosis  and  myocarditis  can 
also  produce  cardiac  pains. 

Another  group  of  symptoms  is  that  due  to  cardiac  decompensation. 
This  is  not  necessarily  a  marked  clinical  feature;   in  fact,  in  three  of 


190  CLINICAL  CARDIOLOGY 

the  cases  it  consisted  only  of  slight  dyspnoea  upon  exertion.  Its  pres- 
ence seems  due  to  accompanying  cardiovascular  disease  rather  than  to 
the  aortic  dilatation  itself.  Edema  is  usually  slight  and  confined  to 
the  legs ;  it  is  extreme  only  in  neglected  cases  or  late  in  the  disease. 
Dyspnoea  is  of  the  usual  cardiac  type ;  it  is  generally  most  marked  on 
exertion ;  it  is  continuous  in  the  severe  cases  with  cardiac  failure.  Left 
ventricular  hypertrophy  of  varying  degrees  is  usually  present.  The  heart 
is  occasionally  tremendously  hypertrophied  before  cardiac  failure  sets  in. 
Diagnosis.  —  The  diagnostic  criteria  of  aneurismal  dilatation  of  the 
arch  and  ascending  aorta  have  frequently  been  emphasized,  particu- 
larly the  rough  systolic  murmur  and  the  accentuated,  ringing  second 
sound  at  the  right  base.  In  dilatation  of  the  descending  aorta  abnormal 
sounds  in  typical  instances  are  best  heard  at  the  left  sternal  border 
at  its  middle  third,  or  from  the  third  left  intercostal  space  to  the  ensi- 
form.  This  is  approximately  the  site  of  the  projected  dilatation  upon 
the  chest  wall.  The  area  of  propagation  of  the  murmurs  is  somewhat 
similar  to  that  occasionally  found  in  valvular  aortic  regurgitation. 
The  signs  outlined  —  the  impact  area,  the  rough  first  and  accentuated 
or  liquid  second  sounds  —  will  usually  serve  as  differential  guides. 
There  is  in  addition,  in  the  aneurisimal  dilatation  described,  a  rough 
systolic  murmur  over  the  dilated  aortal  area.  The  second  sound  has  a 
liquid  rather  than  an  accentuated  tone,  and  is  prolonged  through  the 
entire  diastole  or  is  followed  by  a  diastolic  murmur  of  varying  intensity. 
Although  this  double  murmur  is  the  rule,  the  only  auscultatory  dif- 
ference may  be  a  slightly  impure  first  and  a  somewhat  accentuated 
second  sound.  By  placing  the  eye  upon  a  level  with  the  patient's  chest 
a  distinct  heaving  area  distinguishable  from  that  at  the  apex,  and  oc- 
cupying the  lower  left  sternal  intercostal  spaces,  can  often  be  detected. 
A  sensation  of  impact  is  also  given  to  the  bell  of  the  stethoscope  when, 
during  the  usual  clinical  examination,  it  is  placed  over  this  area.  This 
impact  sensation  is  particularly  well  detected  by  snugly  pressing  two  or 
three  fingers  in  the  left  middle  interspaces  near  the  sternum.  Occa- 
sionally a  systolic  thrill  is  also  palpable.  All  these  signs  are  made  more 
evident  by  having  the  patient  hold  his  breath  at  the  end  of  expiration. 
In  addition  an  interval  in  the  time  of  thrust  between  the  apical  and 
left  intercostal  area  is  sometimes  noted  by  placing  one  finger  over  the 
apex  and  another  over  the  left  sternal  border.  Since,  however,  this 
interval,  physiologically,  comprises  .07  second,  it  may  be  impossible  to 
distinguish  it  by  palpation.  Another  method  for  detecting  this  dif- 
ference is  the  use  of  a  differential  stethoscope,  i.e.  an  ordinary  pair  of 
ear  tubes  arranged  with  two  bells,  one  over  the  apex  and  the  other  over 
the  dilated  aorta.  When  the  murmurs  are  not  too  loud,  the  difference 
in  time  impact  can  thus  be  determined.  The  writer  has  also  attempted 
to  establish  this  difference  by  placing  two  receiving  cups  of  a  polygraph 
over  these  areas  and  noting  the  time  of  arrival  of  the  thrusts  by  the  writ- 
ing pens  upon  the  polygraphic  paper,  but  the  results  were  inconclusive. 


CARDIAC   SYPHILIS  191 

Differential  Diagnosis.  —  It  is  important  to  distinguish  the  aortic 
impacts  to  the  left  of  the  sternum  from  those  found  in  patients  with 
marked  left  ventricular  hypertrophy  or  in  healthy  individuals  with 
overacting  hearts  and  thin  chest  walls.  However,  the  auscultatory 
signs  above  described  are  then  absent.  Although  there  are  many  re- 
finements of  percussion  methods  used  in  the  attempt  to  delicately  out- 
line the  dilated  arch  and  ascending  aorta  (for  example,  threshold  and 
auscultatory  percussion,  Chapter  X)  their  value  in  dilatation  of  the 
descending  aorta  seems  exceedingly  problematical,  because  the  aorta  is 
deep  seated  and  most  of  the  enlarged  area  is  situated  behind  the  ven- 
tricles. An  examination  of  the  posterior  chest  wall  also  fails  to  reveal 
any  difference  from  the  normal  physical  signs.  In  three  of  my  cases 
in  whom  a  correct  tentative  diagnosis  was  made  before  fluoroscopy, 
all  methods  of  percussion  failed  to  reveal  any  enlargement  of  the 
descending  aorta.  To  clinch  the  diagnosis,  examinations  by  means  of 
the  fluoroscope  or  roentgenograms  are  essential.  As  in  examination 
for  suspected  disease  of  other  portions  of  the  aorta,  the  patient  should 
be  fmoroscoped  in  several  lateral  positions.  Fluoroscopy  must  be 
practiced  carefully  in  order  to  reveal  and  distinguish  the  darker 
silhouette  of  the  dilated  descending  aorta  behind  the  left  ventricle. 
Roentgen-ray  plates  must  also  be  carefully  scrutinized  for  the  same 
reason.  It  is  important  in  this  connection  to  again  indicate  the 
differences  in  shadow  areas  between  orthodiascopic  fluoroscopy  and 
roentgenograms  of  the  heart  and  aorta.  It  has  been  my  experience 
that  the  former  produce's  very  little  distortion  in  the  size  of  the  cardiac 
and  aortal  areas,  because  the  X-ray  tube  and  screen  move  together 
and  thus  approximately  parallel  rays  reach  the  observer.  In  the 
roentgenogram,  in  which  the  rays  are  always  divergent,  there  is  an 
increased  cardiac  shadow.  Comparisons  between  the  orthodiascopic 
tracings  and  roentgenograms  in  my  series  of  cases  occasionally  showed 
marked  discrepancies  in  the  size  of  the  dilated  aorta  and  heart. 

Therapy.  —  Treatment  may  be  conveniently  divided  into  three 
parts :  that  of  the  underlying  disease,  of  the  decompensation,  and  of 
the  pains.  The  majority  of  cases  of  aortic  disease  are  known  to  be  of 
luetic  origin,  the  Wassermann  reaction  being  positive  in  most  instances. 
Salvarsan  was  originally  considered  contraindicated  by  Ehrlich  in 
cardiac  lues  because  of  the  fear  of  overwhelming  the  system  with  spiro- 
chetes (Herxheimer  reaction) ;  but  experience  has  shown  that  the  drug 
judiciously  administered  is  definitely  indicated  in  this  disease.  Three 
of  the  cases  here  reported  were  thus  treated  with  excellent  results. 
The  best  routine  procedure  is  the  intravenous  injection  of  .2  gm.  of 
salvarsan  every  week  until  three  doses  have  been  given ;  then,  if  indi- 
cated, it  may  be  repeated  in  .6  gm.  doses  a  month  or  two  apart.  In 
the  interim,  intramuscular  injections  of  mercury  about  twice  weekly 
should  be  given  in  conjunction  with  iodide  of  potash.  If  the  luetic 
changes  in  the  aorta  are  such  that  calcification  and  scar-tissue  formation 


192  CLINICAL  CARDIOLOGY 

are  extensive  and  the  myocardium  is  the  seat  of  advanced  disease,  the 
treatment  can  naturally  be  of  little  or  no  avail.  The  degree  and  extent 
of  such  pathological  changes  cannot  be  diagnosed  accurately  enough 
by  our  present  methods,  although  Vaquez  and  Bordet  claim  to  have 
observed  with  the  fmoroscope  calcified  areas  in  the  ascending  and 
transverse  aorta,  and  the  diminution  of  these  areas  after  salvarsan  in- 
jections. Since  the  treatment  outlined  is  often  efficacious  and  is  fol- 
lowed by  marked  improvement,  I  believe  it  should  be  carried  out  in  all 
cases  unless  the  patient  is  in  extremis.  Even  if  the  Wassermann  re- 
action is  negative,  the  same  therapy  should  be  instituted,  because  syph- 
ilis is  the  preponderatingly  etiological  factor  of  extensive  aortitis,  and 
because  in  any  case  salvarsan  is  not  followed  by  serious  results.  Be- 
sides, a  Wassermann  reaction  which  upon  the  first  examination  is 
negative  may  later  become  positive  even  though  no  provocative  in- 
jections had  been  given ;  this  happened  in  one  of  my  cases. 

Cardiac  failure  accompanying  dilatation  of  the  descending  aorta  re- 
quires the  same  treatment  as  that  from  any  other  cause.  A  reliable 
preparation  of  digitalis  should  be  given.  I  prefer  the  tincture  ad- 
ministered undiluted  in  15-drop  doses  three  times  daily.  If  the  case  is 
urgent  and  very  little  or  no  digitalis  had  previously  been  given,  1  cc. 
of  a  1  per  cent  solution  of  strophanthin  can  be  slowly  injected  intra- 
venously. The  objection  that  digitalis  in  therapeutic  doses  raises  blood 
pressure  has  been  sufficiently  disproved  by  recent  careful  investigations 
(Chapter  XVI).  Digitalis  had  no  effect  upon  the  blood  pressure  in 
any  of  my  cases ;  the  pressure  was  as  often  lowered  as  raised  during 
its  administration.  Symptomatic  treatment  of  the  pains  occasionally 
requires  codein  or  morphine,  but  they  are  frequently  relieved  by  the 
antiluetic  treatment  which  acts  by  controlling  the  inflammatory  ex- 
acerbations of  aortitis  and  periaortitis. 

Prognosis.  —  Dilatation  of  the  descending  thoracic  aorta  is  fre- 
quently overlooked ;  in  fact,  except  in  the  course  of  a  routine  roentgen- 
ray  examination  of  the  chest,  its  diagnosis  by  ordinary  clinical  methods 
has,  to  my  knowledge,  never  previously  been  made.  If  the  patient 
seeks  advice  before  severe  decompensation  sets  in,  and  if  then  the 
condition  is  correctly  diagnosed  and  vigorous  antiluetic  treatment 
instituted,  the  patient  may  live  in  comparative  comfort,  for  the  aortal 
disease  is  an  index  of  the  general  cardiovascular  mischief  rather  than  in 
itself  the  cause  of  cardiac  failure.  Of  the  three  patients  with  slight 
symptoms  who  have  been  under  observation  for  one  year  or  more,  two 
are  clinically  well  and  one  much  improved. 

Cure,  in  the  sense  of  a  return  of  the  aorta  to  its  normal  state,  is  im- 
possible ;  but,  as  in  other  organs  the  luetic  disease  can  be  arrested  and 
controlled,  so  the  heart  and  aorta,  although  somewhat  crippled,  may  be 
sufficiently  restored  to  make  the  patient  comfortable.  Rupture  of  the 
dilated  ascending  and  transverse  aorta  is  extremely  infrequent.  Un- 
less the  luetic  disease  is  confined  to  a  small  area,  this  accident  seems 


CARDIAC   SYPHILIS  193 

less  likely  to  occur  in  the  descending  aorta  because  of  its  greater  length 
and  because  the  dilatation  occupies  a  larger  area. 

Because  of  its  importance  I  shall  summarize  the  clinical  complex  of 
aneurismal  dilatation  of  the  descending  aorta  as  I  have  observed  it. 
The  Wassermann  test  was  done  in  four  of  the  five  cases.  It  was  posi- 
tive in  two  and  negative  in  two.  One  of  the  latter  gave  a  definite  his- 
tory of  luetic  infection.  Three  cases  had  slight  symptoms  when  treat- 
ment was  begun ;  these  were  clinically  cured.  One,  with  severe  heart 
failure,  was  much  improved.  In  three  the  correct  diagnosis  was  made 
by  the  presence  of  an  impact  area  to  the  left  of  the  sternum  at  its  mid- 
dle third,  and  by  prominent  localization  of  the  murmurs  over  this  area. 
Electrocardiograms  were  taken  in  four  cases ;  three  showed  complexes 
of  left  ventricular  preponderance,  the  fourth  was  normal.  The  physical 
signs  of  all  the  cases  were  most  marked  when  the  symptoms  — dyspnoea, 
pain,  or  cardiac  failure  —  were  present ;  the  signs  became  less  with 
improvement. 

In  conclusion  it  may  be  stated  that  aneurismal  dilatation  may  be 
confined  to  the  descending  thoracic  aorta  alone;  it  may  then  occasion 
sufficiently  definite  physical  signs  to  lead  to  its  tentative  diagnosis  by 
the  ordinary  methods  of  clinical  examination.  The  physical  signs  are 
most  prominent  to  the  left  of  the  sternum  at  its  middle  third.  Roent- 
gen-ray investigation  is  indispensable  for  a  positive  diagnosis.  The 
symptoms  are  often  very  slight.  The  disease  may  run  a  mild  course, 
lasting  many  years.  Intensive  antiluetic  treatment  —  salvarsan,  mer- 
cury, and  iodide  of  potash  —  is  indicated  in  every  case. 

REFERENCES 

Chapter  XIV 

Adami  and  Nicholls  :  Principles  of  Pathology,  2d  Edition,  178. 

Allbutt's  System  of  Medicine,  VI,  658. 

Einthoven,   W. :    Weiteres  ueber  das   Elektrokardiogram ;    Archive  fuer   die 

gesammte  Physiologie,  1908,  CXXII,  517. 
Gruber,  G.  B. :  Ueber  die  Doehle-Hellerische  Aortitis. 
Held,  I.  W. :  Aortitis  Syphilitica;  Medical  Record,  1913,  LXXXIV,  1105. 
Hodgson,  J. :  Treatment  of  Diseases  of  the  Arteries  and  Veins,  1815. 
Kraus,  F. :  Ueber  die  Aortenerweiterung  bei  der  Heller-Doehleschen  Aortitis ; 

Deutsche  Medizinische  Wochenschrift,  1914,  XL,  577. 
Lewis,  T. :   Observations  on  Ventricular  Hypertrophy,  etc. ;  Heart,  1914,  V,  367. 
Longcope,  T.  W. :  Syphilitic  Aortitis  —  Its  Diagnosis  and  Treatment ;  Archives 

of  Internal  Medicine,  XI,  15. 
McCrae,  T. :  Dilatation  of  the  Aorta  ;  American  Journal  of  the  Medical  Sciences, 

1910,  CXL,  469. 
Mackenzie,  J. :  Digitalis;  Heart,  1910-1911,  II,  284. 
Manoelian,  Y. :  Recherches  sur  le  plexus  cardiaque,  etc. ;  Annalen  de  l'lnstitut 

Pasteur,  June,  1914,  579. 
Osier's  System  of  Medicine,  IV,  457. 
Price,  F.  W. :    Some  Investigations  on  the  Action  of  Digitalis  on  the  Blood 

Pressure  in  Man  ;  British  Medical  Journal,  1912,  II,  689. 
Thoma,    R. :    Untersuchungen  ueber  Aneurismen ;    Virchow's  Archiv,    1888, 

CXI,  89. 
Vaquez  et  Bordet :   Le  Cceur  et  L'Aorte. 
Vaquez,  H.,  et  Laubry,  C. :    Sur  le  Traitement  Specifique  des  Aortites,   etc. ; 

Archives  des  Maladies  du  Cceur,  1912,  V,  561. 


CHAPTER  XV 

SYMPTOMATOLOGY,  PHYSICAL  SIGNS,  DIAGNOSIS  AND 
PROGNOSIS  OF  MYOCARDITIS  AND  OF  CARDIOSCLE- 
ROSIS 

From  a  description  of  the  pathological  changes  found  in  myocarditis 
(Chapter  XII),  it  becomes  apparent  that  the  symptomatology  must  be 
a  varied  one,  and,  to  a  great  extent,  must  depend  upon  the  type  and 
extent  of  the  pathological  process. 

It  is  important  to  remember  that  the  diagnosis  of  myocarditis, 
when  present  alone,  is  often  extremely  difficult  or  even  impossible. 
Often,  the  diagnosis  must  be  made  from  the  symptoms  of  myocardial 
insufficiency.  Myocarditis  rarely  exists  as  an  isolated  pathological 
lesion.  It  is  usually  combined  to  a  varying  degree  with  the  patho- 
logical ensemble  characteristic  of  cardiosclerosis,  the  physical  signs  of 
which  are  much  more  definite  and  more  readily  recognizable  than  those 
of  myocarditis  alone. 

The  physical  signs  of  myocarditis  as  an  isolated  entity  may  be  limited 
to  some  evidence  of  enlargement  of  the  heart,  or,  in  advanced  cases, 
of  severe  degeneration,  to  weakness  of  the  first  sound  at  the  base 
and  apex,  and  to  weakness  or  entire  absence  of  the  second  sound,  es- 
pecially at  the  base.  From  the  physical  examination  alone  it  may  not 
be  possible  to  venture  more  than  a  guess  as  to  the  extent,  or  even  the 
presence,  of  any  myocardial  damage.  When  considered,  however, 
in  conjunction  with  such  other  data  as  furnished  by  the  etiological 
factor,  the  size  of  the  heart,  the  condition  of  the  palpable  arteries,  the 
absence  of  valvular  disease,  the  presence  of  muffled  and  indistinct  cardiac 
sounds,  moderate  tachycardia  with  dyspnoea,  the  subjective  and  ob- 
jective phenomena  indicative  of  myocardial  insufficiency,  it  may  be 
possible  to  state,  with  a  fair  amount  of  accuracy,  the  extent  of  myo- 
cardial mischief.  It  is  clear,  then,  that  the  diagnosis  must  often  be 
established  inferentially  and  by  exclusion. 

With  reference  to  cardiosclerosis,  if  the  morbid  process  is  at  all 
advanced,  it  is  readily  diagnosed  from  the  physical  signs.  Prominent 
among  these  are  the  signs  of  aortitis.  If  the  latter  is  accompanied 
by  simple  or  aneurismal  dilatation  of  the  arch  of  the  aorta,  one  often 
finds,  on  inspection,  a  broad  expansile  rise  of  the  tissues  in  the  supra- 
sternal notch,  due  to  the  vigorous  overaction  and  enlargement  of  the 

194 


MYOCARDITIS  AND   CARDIOSCLEROSIS  195 

arch.  In  advanced  cases  of  arteriosclerosis  the  carotid  arteries  may  be 
tortuous  and  thickened  and  may  pulsate  very  vigorously  and  with  an 
accentuated  thrust.  If  the  first  part  of  the  aorta  is  especially  involved  in 
the  degenerative  process,  the  carotid  phenomenon  may  be  more  marked 
on  the  right  than  on  the  left  side.  In  a  thin-chested  individual,  with 
the  patient  lying  prone,  and  with  the  eye  of  the  observer  on  a  level 
with  the  patient's  chest,  it  is  sometimes  possible  to  see  the  tissues  over 
the  right  second  interspace  pulsate  in  simple  or  aneurismal  dilatation 
of  the  aorta.  The  fluoroscopic  and  orthodiascopic  aspects  of  these 
lesions  (Chapter  IX),  and  the  difficulty  of  mapping  out  the  aortal 
limits  by  physical  examination  (Chapter  X),  have  already  been  described. 

Corresponding  to  the  physical  signs  discovered  by  inspection,  on 
palpation  there  is  a  marked  thrust  felt  by  lightly  insinuating  the  finger 
behind  the  sternum ;  a  similar  thrust  may  be  found  over  the  carotids. 
Systolic  expansion  over  the  right  base  may  likewise  be  felt  by  snugly 
applying  the  fingers  laid  flatly  in  the  second  and  third  right  interspaces 
near  the  sternum. 

The  auscultatory  signs  of  typical  aortitis  are  characteristic  and 
readily  recognized.  The  first  sound  is  rough  and  harsh;  the  second, 
accentuated,  and,  in  some  instances,  metallic  and  tinny  in  character. 
The  latter  has  usually  been  interpreted  as  due  to  hypertension, 
a  frequent  accompaniment  of  aortitis.  It  is  fairly  frequent,  however, 
when  hypertension  is  not  present.  Acoustically,  it  seems  probable 
that  the  metallic  tone  is  at  least  partly  due  to  dilatation  of  the  aorta, 
as  already  described  (Chapter  XIV).  The  roughened  and  harsh  first 
sound  is  occasionally  heard  by  placing  the  stethoscope  in  the  jugulum 
over  the  pulsating  arch ;  this  phenomenon  depends  partly  upon  the 
extent  of  aortic  enlargement  and  partly  upon  the  height  of  the  aortic 
arch.  The  murmur  is  sometimes  propagated  along  the  carotids.  Fol- 
lowing the  second  sound,  a  diastolic  murmur  of  varying  duration  and 
intensity  may  be  heard  over  the  right  base.  It  is  usually  transmitted 
downwards  along  the  right  sternal  border  ;  it  is  on  rare  occasions  heard 
best  over  the  third  left  interspace  and  along  the  left  sternal  border. 

Although  the  physical  signs  above  described  are  characteristic  and 
typical  of  aortitis,  there  is  scarcely  a  cardiac  lesion  which  produces 
more  varied  or  atypical  auscultatory  phenomena.  For  example,  the 
sounds  may  be  perfectly  normal  at  the  right  base,  the  first  or  second 
sounds  or  both  may  be  extremely  faint  or  entirely  absent.  Upon  what 
changes  in  the  aorta  such  differences  depend  it  is  at  this  time  impossible 
to  state. 

The  sounds  that  are  heard  at  the  apex  are  rarely  significant  in  the 
diagnosis  of  aortitis.  They  apparently  vary  with  the  state  of  efficiency 
of  the  circulation,  and,  to  a  lesser  extent,  with  the  state  of  hypertension. 
For  example,  the  first  sound  may  be  unclear  and  muffled,  or  entirely 
absent.  Occasionally,  in  cases  of  hypertension,  with  or  without  left 
ventricular  hypertrophy,  the  second  sound  at  the  apex  takes  on  char- 


196  CLINICAL   CARDIOLOGY 

acteristics  similar  to  that  at  the  right  base,  i.e.  it  becomes  metallic  in 
tone.  In  conjunction  with  a  weak  or  absent  first  sound,  the  cardiac 
impact  may  be  weak  or  scarcely  palpable.  One  instance  characteristic 
of  these  findings  I  was  able  to  prove  at  necropsy.  The  patient  com- 
plained of  severe  epigastric  pains,  especially  on  walking.  The  cardiac 
examination  showed  a  muffled  first  sound  over  the  right  base  and  a 
scarcely  perceptible  first  sound  at  the  apex.  Polygraphic  tracings 
showed  heart  block.  The  orthodiascope  tracing  showed  enlargement 
of  the  first  part  and  arch  of  the  aorta,  and  an  enlarged  left  ventricle. 
The  patient  died  suddenly.  At  necropsy,  there  was  diffuse  dilatation 
and  thickening  of  the  aorta  from  its  root  to,  and  including,  the  upper 
abdominal  aorta ;  spirochetes  were  isolated  from  the  aortal  wall.  There 
was  moderate  left  ventricular  hypertrophy ;  the  myocardium  was  riddled 
with  scar  tissue. 

While  physical  signs  like  those  I  have  described  are  suggestive  of 
myocarditis  and  aortitis,  these  lesions  can  be  present  and  yet  sounds 
at  the  apex  and  base  be  perfectly  normal.  A  faint  systolic  murmur 
may  accompany  the  first  sound ;  this,  however,  possesses  no  diagnostic 
value,  for  such  impurities  are  by  no  means  rare  in  normal  hearts.  Of 
much  more  significance  is  the  presence  of  a  loud  and  rough  systolic 
murmur  heard  most  prominently  at  the  apex,  and  sometimes  trans- 
mitted to  the  left.  These  murmurs  are  probably  caused  by  fibrous 
or  calcareous  valvular  thickening  (Chapter  XII)  with  consequent 
mitral  regurgitation  (Chapter  X).  In  old  individuals  with  marked  senile 
arteriosclerosis  and  widespread  aortic  and  valvular  changes  —  a 
cardiovascular  condition  also  found  occasionally  in  the  adult  —  there 
is  sometimes  heard  a  very  loud,  rough,  systolic  murmur  over  the  entire 
anterior  part  of  the  chest ;  this  murmur  is  transmitted  to  the  left,  and 
may  even  be  heard  posteriorly  between  the  spines  of  the  scapulae.  In 
its  harshness,  loudness,  and  area  of  transmission,  it  is  extremely  sug- 
gestive of  aneurism  ;  however,  a  diastolic  murmur  is  rarely  encountered 
and  the  roentgenograms  of  the  cases  that  I  have  studied  have  not  regu- 
larly shown  abnormal  aortic  enlargement.  This  loud  systolic  mur- 
mur is  apparently  the  result  of  the  coalescence  of  two  components :  an 
aortic  systolic  and  a  mitral  regurgitant  murmur.  The  aortic  factor  is 
either  atheromatous  change  in  the  aortic  flaps  producing  stenosis,  or 
the  impact  of  the  blood  stream  over  the  roughened  sclerotic  aortal  wall ; 
both  causes  sometimes  operate  together  to  produce  this  aortic  com- 
ponent. The  mitral  component  of  the  murmur  is  due  to  sclerotic 
changes  in  the  mitral  cusps.  The  intensity  of  the  combined  murmur 
seems  to  depend  upon  the  state  of  myocardial  efficiency.  I  have  found 
it  exceptionally  loud  only  in  those  who  were  compensated,  or  in  whom 
there  was  but  slight  cardiac  failure.  On  the  other  hand,  this  murmur 
may  be  absent  in  those  who  clinically  or  at  necropsy  show  advanced 
cardiosclerotic  changes.     Such  an  instance  is  the  following : 

A  robust  man  of  44  complained  chiefly  of  substernal  pains  upon 


MYOCARDITIS  AND   CARDIOSCLEROSIS  197 

slight  exertion.  There  were  occasional  attacks  of  nocturnal  dyspnoea. 
The  only  abnormality  upon  auscultation  was  slight  muffling  of  all  the 
cardiac  sounds.  Several  Wassermann  blood  tests  were  negative.  The 
patient  finally  died  of  myocardial  insufficiency.  At  necropsy,  incrusted 
calcareous  deposits  were  found  on  all  the  valves.  The  coronaries  were 
thickened  and  impermeable,  the  aortal  arch  was  markedly  atheromatous, 
the  myocardium  contained  many  fibrous  patches.  As  already  suggested, 
the  absence  of  loud,  harsh  murmurs  in  this  case  was  probably  due  to 
failing  circulation. 

An  extremely  valuable  hint  regarding  the  degree  of  cardiosclerotic 
change  is  sometimes  given  by  the  presence  of  pericardial  adhesions. 
These  are  found  most  frequently  over  the  right  base  or  in  the  apical 
region.  Superficial  creaking  sounds  or  pericardial  rubs  are  then  heard 
at  the  end  of  long  inspiration,  or  accompanying  cardiac  systole.  The 
importance  of  diagnosing  these  old  localized  adhesions  lies  not  so  much 
in  the  fact  that  they  add  embarrassment  to  the  circulation,  but  because 
they  are  found  only  when  the  cardiosclerotic  changes  are  very  advanced. 
Thus  far,  most  stress  in  the  diagnosis  of  cardiosclerosis  has  been 
laid  upon  the  auscultatory  signs.  Other  important  diagnostic  data 
may  be  gained  by  examination  for  ventricular  hypertrophy,  hyperten- 
sion, and  palpable  and  audible  reduplicated  first  sounds  at  the  apex. 
The  significance  and  bearing  of  all  these  phenomena  are  more  fully 
described  in  their  appropriate  connections. 

Symptomatology  of  Cardiosclerosis.  —  As  the  morphology  of  car- 
diosclerosis is  a  varied  one,  so  its  symptomatology  depends  upon  the 
factor  that  is  clinically  predominant.  It  is  evident  that  it  is  often  im- 
possible to  group  these  patients  into  one  class,  for  the  symptoms  pro- 
duced by  the  various  underlying  pathological  changes  overlap.  It 
has  already  been  pointed  out,  for  example,  that  arteriolar  and  capillary 
fibrosis  may  be  a  generalized  pathological  process,  or  may  attack  in- 
dividually the  arterial  system  of  the  heart,  the  kidneys,  or  the  brain. 
In  such  types,  the  symptoms  are  respectively  predominantly  cardiac, 
renal,  or  cerebral.  We  shall  here  concern  ourselves  only  with  those 
individuals  in  whom  the  cardiac  symptoms  form  the  chief  complaint. 
As  with  other  cardiac  patients,  the  earliest  subjective  symptom  is  usually 
dyspnoea.  Its  onset  is  gradual  and  evident  at  first  only  after  severe 
exertion.  Later,  the  dyspnoea  occurs  upon  slight  exertion.  It  is  fre- 
quently associated  with  a  sense  of  weight  or  oppression  on  the  chest, 
at  first  transient,  and  later  constant.  These  sensations  must  be  dif- 
ferentiated from  the  precordial  pain  and  distress  (Chapter  XXI)  from 
which  such  patients  also  suffer.  Precordial  pains  may  be  slight  and 
localized,  or  severe  and  radiate  to  the  left  axilla  and  arm,  to  the  neck, 
interscapular  region,  or  occasionally  to  the  right  arm.  At  first  the  pains 
occur  after  exertion;  later,  they  may  appear  in  attacks  which  rouse 
the  patient  from  a  sound  sleep.  Slight  hemoptyses  occurring  after 
exertion  sometimes  antedate  the  subjective  symptoms  for  months  or 


198  CLINICAL  CARDIOLOGY 

even  years.  An  enlarged,  congested  liver,  smooth  and  globular  in  out- 
line, is  another  objective  symptom  which  may  be  found  before  the 
patient  complains  of  dyspnoea.  It  is  not  uncommon  to  feel  the  edge 
of  the  liver  several  inches  below  the  free  border  of  the  ribs.  Epigastric 
sensitiveness  to  pressure  is  fairly  frequent.  It  is  found  even  when  the 
liver  is  not  enlarged.  The  cause  is  usually  assumed  to  be  congestion 
of  the  gastric  mucous  membrane ;  in  another  connection,  I  have  pointed 
out  that  it  is  probably  of  reflex  origin,  the  source  primarily  being  excita- 
tion of  the  cardiac  nerves. 

Pulmonary  examination  often  reveals  crepitant  rales  at  both  bases. 
Their  presence  is  prognostically  suggestive  of  subsequent  attacks  of 
pulmonary  edema.  The  latter  may  be  mild  and  recur  frequently,  or 
a  very  severe  attack  may  suddenly  take  place  after  unusual  exertion  or 
excitement.  Hydrothorax,  usually  right-sided,  may  also  be  present. 
Edema  of  the  legs  is,  at  the  outset,  only  slight,  and  is  usually  present 
after  the  patient  has  been  up  and  about,  unless  the  process  is  far  ad- 
vanced and  has  not  responded  to  therapy. 

The  types  of  arrhythmias  encountered  in  cardiosclerosis  are  of  some 
clinical  significance.  Those  found  in  senile  cases  will  be  discussed  later. 
When  decompensation  is  not  far  advanced,  the  pulse  is  regular.  Ex- 
trasystoles  usually  represent  the  first  type  of  arrhythmia  to  appear ; 
they  are  mostly  of  the  ventricular  variety.  The  next  most  frequent 
type  is  auricular  fibrillation.  Heart  block  is  usually  found  only  in 
advanced  cases.  In  isolated  instances,  attacks  of  paroxysmal  tachy- 
cardia alone,  or  alternating  with  auricular  fibrillation,  are  found.  In 
one  case,  for  example,  a  man  of  54  with  moderate  hypertension,  mild 
cardiosclerosis,  and  slight  precordial  pain,  there  was  an  attack  of  par- 
oxysmal tachycardia  lasting  one  week ;  thereafter  the  patient  felt  well 
for  several  months.  He  then  developed  auricular  fibrillation,  again 
accompanied  by  only  slight  precordial  discomfort.  This  attack  lasted 
four  days.  The  patient  was  feeling  quite  comfortable,  and  his  condi- 
tion was  apparently  progressing  favorably.  While  sitting  in  a  chair  the 
patient  suddenly  died.  In  neither  attack  was  dyspnoea  severe  or  a 
prominent  symptom.  In  some  patients  the  cardiac  irregularities  change 
suddenly,  and  apparently  capriciously,  from  one  type  to  another,  es- 
pecially from  extrasystoles  to  auricular  fibrillation,  or  vice  versa.  An 
example  has  just  been  quoted.  Such  variability  I  have  found  of  ominous 
prognostic  import. 

There  exists  a  small  group  of  patients  in  whom  digitalis  does  not  re- 
lieve decompensation,  but  produces  diverse  arrhythmias  in  rapid  suc- 
cession; these  are  chiefly  sinus  arrhythmia  and  extrasystoles,  either 
isolated  or  coupled.  Here,  too,  I  have  found  that  the  occurrence  of 
such  varied  arrhythmias  may  portend  a  fatal  outcome  within  a  few  weeks 
or  months. 

In  patients  with  senile  cardiosclerosis,  —  that  is,  those  who  have  in 
addition  to  cardiosclerotic  changes   palpably  thickened  and  tortuous 


MYOCARDITIS  AND   CARDIOSCLEROSIS  199 

arteries,  —  auricular  fibrillation  is  very  common.  One  of  my  hospital 
services  consists  of  old  people  with  and  without  cardiovascular  symp- 
toms ;  among  these  there  is  a  large  proportion  of  fibrillators.  In  those 
who  are  compensated,  the  cardiac  rate  is  usually  between  70  and  80  per 
minute,  most  of  the  beats  being  effective  and  reaching  the  wrist.  In 
those  who  suffer  from  severe  decompensation  the  cardiac  activity  is 
rapid  and  quite  irregular,  with  many  frustrane  beats.  The  course  of 
the  elderly  cardiosclerotic  patient  is  essentially  afebrile,  unless  disturbed 
by  complications.  Of  these  the  most  frequent  consist  in  attacks  of 
pneumonia,  the  majority  of  which  are  of  hypostatic  or  embolic  origin. 

Prognosis  in  Cardiosclerosis 

Under  this  caption  are  included  those  non-rheumatic  chronic  cases 
of  heart  disease  which  show  various  degrees  of  involvement  of  the 
myocardium,  and  atheromatous  changes  of  the  endocardium,  the  cor- 
onaries,  the  valves,  and  the  aorta.  With  the  exception  of  syphilis, 
the  bacterial  infection  or  chemical  poison  has  long  since  reached  the 
quiescent  stage ;  the  pathological  process,  however,  in  most  instances 
insidiously  and  slowly  continues.  Clinical  and  pathological  proof  of 
this  is  usually  lacking,  since  the  slow  progress  of  the  damage  can 
scarcely  show  itself  except  by  careful  clinical  observation  of  the  same 
patient  over  a  long  period  of  time,  or  by  occasional  necropsies  of 
patients  in  whom  the  disease  had  been  watched  and  studied  since  its 
incipiency. 

The  kind  and  frequency  of  complications  found  in  cardiosclerosis  are, 
in  the  main,  different  from  those  in  rheumatic  endocarditis.  Prognos- 
tically,  much  depends  upon  the  type  of  disease  which  dominates  the 
clinical  ensemble.  For  example,  if  the  uremic  element  predominates, 
the  prognosis  will  revolve  upon  that;  cerebral  hemorrhage  or  acute 
uremia  are  then  apt  to  be  the  commoner  ways  in  which  the  disease  will 
terminate.  If  arteriosclerotic,  the  terminal  accidents  are  prone  to  be 
hemiplegias  or  monoplegias.  But  the  arteriosclerotic  syndrome  itself 
can  occasionally  be  clinically  subdivided  into  that  affecting  the  aorta 
and  the  coronary  circulation,  and  that  involving  the  myocardium ; 
the  prognosis  must  then  be  studied  from  these  separate  standpoints. 

General  Prognosis.  —  '  Acute  accidents  '  which  may  occur  and 
which  naturally  immediately  change  the  entire  prognostic  picture  will 
be  discussed  later.  Aside  from  these,  the  general  prognosis  depends 
upon  an  attempt  to  gauge  the  rate  of  development  and  extent  of  car- 
diosclerotic damage,  and  the  actual  degree  of  myocardial  insufficiency. 
The  first  is  only  derived  from  careful  and  patient  inquiry  into  the 
onset  of  cardiovascular  symptoms  and  from  tangible  evidence  of  an 
underlying  infective  process.  From  these  the  duration  of  the  disease 
may  be  estimated.  For  example,  in  one  instance  of  severe  myocarditis 
with  decompensation  in  a  physician  of  55,  I  was  definitely  able  to 


200  CLINICAL  CARDIOLOGY 

establish  the  commencement  of  the  disease  as  a  mild  nephritis  following 
grippe  infection  some  20  years  previously.  This  the  patient  had  entirely 
overlooked  as  being  of  no  etiological  significance.  Very  slight  cardiac 
symptoms  began  15  years  ago.  They  consisted  of  slight  dyspnoea  and 
occasional  hemoptyses.  Acute  symptoms  of  decompensation  appeared 
only  a  few  months  ago ;  they  usually  occurred  after  rapid  walking  or 
after  coitus.  The  fact  that  cardiac  symptoms  began  15  years  ago, 
and  the  present  status  of  widespread  cardiosclerosis  as  revealed  upon 
examination,  make  it  appear  that  the  pathological  damage  must  have 
long  antedated  the  symptoms.  The  entire  history  speaks  for  a  steady 
though  very  gradual  continuation  of  the  pathological  mischief.  This 
case  well  illustrates  the  meaning  conveyed,  and  the  information  to  be 
gained,  by  a  careful  clinical  history,  in  an  attempt  to  roughly  approxi- 
mate not  only  the  degree  of  cardiovascular  disease  but  the  length  of 
time  required  to  reach  the  condition  found  when  the  patient  first  pre- 
sents himself  for  examination.  The  degree  of  myocardial  insufficiency 
is  gauged  not  only  by  physical  signs,  but  also  by  its  usual  clinical  man- 
ifestations ;  these  are  chiefly  dyspnoea,  precordial  distress,  and  a  sense 
of  exhaustion  after  effort. 

It  will  be  noted  that  the  amount  of  cardiac  hypertrophy  and  of  hy- 
pertension have  not  been  emphasized  because  they  are  more  concerned 
with  sudden  heart  failure  and  cerebral  accidents  than  with  the  ques- 
tion of  '  general  prognosis.'  Thus,  specimens  of  extremely  hyper- 
trophied  and  diseased  hearts  have  been  removed  from  patients  who 
lived  to  ripe  old  age,  and  in  whom  the  disease  had  doubtless  been 
present  for  many  years.  So,  too,  clinicians  have  for  many  years 
followed  patients  who  had  severe  aortal  and  myocardial  involvement, 
some  of  them  proved  as  such  at  necropsy ;  yet  during  this  long  period 
there  may  have  been  no  marked  discomfort  and  almost  negligible  sub- 
jective symptoms  from  the  cardiac  disase. 

With  our  present  knowledge,  we  cannot  state  why  some  tremendously 
hypertrophied  hearts  carry  their  circulatory  burdens  fairly  well  for 
many  years,  while  other  apparently  more  nearly  normal  hearts  suffer 
from  circulatory  failure.  I  would  suggest  that  the  activity  and  degree 
of  the  progress  of  the  pathological  process  play  important  roles.  The 
system  may  accustom  itself  to  a  gradual  curtailment  of  its  circulatory 
reserve,  while  a  more  acute  though  less  widespread  pathological  change 
might  be  attended  by  quick  cardiac  exhaustion  in  a  heart  already  work- 
ing at  or  near  its  maximal  energy. 

In  order  to  study  myocardial  insufficiency  from  the  standpoint  of 
prognosis,  it  is  necessary  to  estimate  not  only  the  amount  of  gross  patho- 
logical damage  to  the  cardiovascular  system,  but  also  the  amount  of 
fairly  healthy  tissue  sufficient  to  carry  on  the  circulation.  For  these 
purposes,  besides  careful  physical  examination,  it  is  necessary  to  exam- 
ine the  cardiac  reserve  power  so  as  to  determine  whether  any  "  factor  of 
safety  "  remains.     Functional  efficiency  tests  (Chapter  XVIII)  may  be  of 


MYOCARDITIS  AND   CARDIOSCLEROSIS  201 

some  value  in  this  connection.  Of  more  aid  and  more  readily  applicable 
are  the  facts  already  mentioned,  which  can  be  determined  by  the 
ordinary  methods  of  clinical  examination.  These  include  the  investiga- 
tion of  the  result  of  effort  and  exercise  upon  the  heart  rate,  the  patient's 
subjective  sensations,  the  size  of  the  liver,  the  presence  of  dyspnoea, 
edema,  hydrothorax,  and  precordial  distress. 

To  study  ideally  the  degree  and  rate  of  progress  of  the  pathological 
damage  requires  a  knowledge  of  the  patient  over  a  number  of  years, 
but  this  opportunity  is  only  exceptionally  vouchsafed  us.  We  shall 
therefore  have  to  depend  in  the  main  upon  the  data  and  history  furnished 
by  the  patient.  Of  great  importance  prognostically  are  the  frequency, 
type,  and  duration  of  attacks  of  decompensation,  and  the  manner  and 
rapidity  with  which  they  yield  to  proper  therapy.  These  considerations 
are  often  glossed  over  or  entirely  disregarded ;  yet  from  them,  in  ad- 
dition to  other  data,  one  is  frequently  correctly  guided  as  to  the  ultimate 
'  general  prognosis.'  Much  will  naturally  depend  upon  the  individual 
opinion  of  what  is  "  proper  therapy."  If,  for  example,  decompensation 
has  been  relieved  after  a  few  days'  rest  and  dosage  with  a  reliable  prep- 
aration of  digitalis,  or  if  edema  has  been  relieved  and  diuresis  promoted 
by  diet  (q.v.)  and  some  caffeine  derivative  (theobromin,  theocin,  caf- 
feine), it  is  safe  to  make  a  good  general  prognosis  regarding  longevity. 
On  the  other  hand,  if  decompensation  is  frequent,  marked,  and  refrac- 
tory to  treatment,  the  general  prognosis  becomes  correspondingly  poor. 

Knowledge  of  the  prognostic  features  included  under  the  term 
Acute  Accidents  depends  upon  the  fact  that,  in  the  pathology  of  cardio- 
sclerosis, there  is  an  admixture  of  myocardial,  arterial,  and  valvular 
disease  in  varying  proportions ;  it  requires  not  only  laboratory  tests  and 
detailed  examination,  but  also  clinical  acumen  and  broad  experience  to 
decipher  and  properly  apportion  the  damage  to  the  heart,  kidneys, 
arteries,  and  brain.  Thus,  aneurismal  dilatations  of  the  aorta  may  be 
confined  to  its  first  portion,  the  arch,  or  to  the  descending  thoracic  aorta, 
and  not  markedly  affect  the  coronaries  or  myocardium.  In  other 
patients  with  cardiosclerosis,  the  coronaries  and  their  branches  are 
only  slightly  involved,  while  the  brunt  of  the  disease  affects  the  myo- 
cardium and  produces  myofibrosis  and  hypertrophy.  Conversely, 
coronary  disease  may  be  widespread  and  include  subsidiary  branches 
of  the  second  and  even  third  order,  yet  the  myocardium  remain  com- 
paratively healthy.  Again,  an  arteriosclerotic  process  may  spend  itself 
chiefly  upon  the  circle  of  Willis,  and  produce  symptoms  of  cerebral 
softening.  All  these  instances  show  how  necessary  it  is  to  search  out 
the  lesion  which  is  symptomatically  and  pathologically  predominant; 
for  in  this  manner  alone  can  a  fairly  scientific  prognosis  be  grounded, 
and  '  acute  accidents '  foretold  and  possibly  guarded  against. 

For  the  purpose  of  studying  acute  accidents  prognostically  patients 
with  cardiosclerosis  may  be  roughly  grouped  into  those  with  predomi- 
nant arteriosclerotic,  uremic,  or  cardiac  symptoms.     In  cases  of  general 


202  CLINICAL  CARDIOLOGY 

atheroma  without  marked  hypertension  (usually  found  in  the  senile), 
the  commoner  sudden  causes  of  death  are  cerebral  hemorrhage,  pneu- 
monia, or  pulmonary  stasis.  The  latter  produces  bubbling  or  crepitant 
rales  at  both  bases.  These  signs  may  be  present  for  weeks  or  months 
before  the  acute  accidents  occur ;  they  help  to  presage  probable  pul- 
monary edema  or  a  terminal  pulmonary  infection. 

A  fairly  definite  hint  of  cardiac  failure  or  of  impending  death  is 
furnished  by  the  presence  of  arrhythmias,  the  type  of  which  change, 
apparently  capriciously,  hourly  or  daily.  Thus,  at  various  times,  extra- 
systoles,  auricular  fibrillation,  or  tachycardia  may  alternate  with  a 
regular  pulse.  This  heightened  ventricular  irritability  is  not  neces- 
sarily associated  with  any  demonstrable  change  in  the  clinical  symptoms. 
It  seems  to  be  due  to  some  profound  change  in  cardiac  nutrition  de- 
pendent upon  severe  sudden  focal  myocardial  damage  from  emboli  or 
infarcts.     The  following  cases  will  serve  to  illustrate  the  clinical  picture. 

Male,  age  fifty-five,  was  suffering  from  mild  nephritis  and  cardio- 
sclerosis with  moderate  hypertension.  The  main  complaint  was  slight 
dyspnoea  upon  climbing  stairs.  He  improved  under  therapy  and  felt 
comparatively  well  for  one  year.  His  pulse  had  always  been  regular 
until  one  day  he  complained  of  constant  "  fluttering  "  in  his  heart. 
Clinical  examination  and  electrocardiograms  showed  a  simple  tachy- 
cardia; the  rate  was  160  per  minute.  His  condition  was  accompanied 
by  very  slight  dyspnoea.  There  was  no  precordial  pain.  The  tachy- 
cardia lasted  two  days.  For  a  period  of  three  months  he  again  felt  well, 
his  pulse  remained  regular.  Then,  suddenly,  during  the  night  he  com- 
plained of  feeling  faint  and  of  very  slight  "  uneasiness  "  in  the  chest. 
Again  slight  dyspnoea  was  present.  Examination  showed  auricular 
fibrillation  with  rapid  and  irregular  heart  action ;  the  cardiac  rate  was 
150  per  minute.  He  was  put  upon  digitalis  and  later  was  allowed  to 
sit  out  of  bed.  The  fibrillation  continued,  but  the  patient  said  he  felt 
very  much  better.  Despite  apparent  improvement  and  absence  of 
pain,  a  diagnosis  of  probable  coronary  infarct  was  made,  and  a  guarded 
prognosis  given  regarding  the  outcome  of  the  attack.  After  four  days, 
while  the  patient  was  sitting  quietly  at  the  table  and  reading,  he  gasped 
and  died  within  two  minutes. 

Female,  age  sixty-seven,  well  preserved,  had  been  complaining  of 
substernal  pain  for  one  year.  More  recently,  she  began  to  have  at- 
tacks of  dyspnoea  and  of  pains  lasting  one  hour  and  radiating  to  the 
back.  At  such  times,  the  pulse  became  "  irregular  "  (auricular  fibril- 
lation?); between  attacks  it  remained  regular.  Upon  examination, 
the  systolic  blood  pressure  was  168,  the  diastolic  80 ;  there  was  slight 
pretibial  edema.  Fluoroscopic  examination  showed  a  somewhat  dilated 
aortic  arch.  The  urine  contained  neither  casts  nor  albumen.  The 
electrocardiographic  tracing  showed  a  few  ventricular  extrasystoles.  A 
diagnosis  of  probable  coronary  sclerosis  was  made  and  sudden  death 
prognosticated,  mainly  because  of  the  arrhythmia  which  accompanied 


MYOCARDITIS  AND   CARDIOSCLEROSIS  203 

the  attacks  of  dyspnoea.  Two  months  after  the  first  examination,  she 
had  an  attack  of  dyspnoea  and  precordial  pain,  and  died  within  a  few 
minutes. 

Prognosis  in  Cardiosclerosis  with  Coronary  Disease.  — Where  disease 
of  the  coronaries  is  assumed  to  be  the  main  cause  of  the  symptoms 
(Chapter  XXI),  the  prognosis  depends  upon  the  severity  of  the  precordial 
attacks  and  upon  the  extent  of  concomitant  cardiac  damage ;  in  other 
words,  upon  the  state  of  preservation  of  the  remainder  of  the  cardio- 
vascular apparatus.  If  compensation  is  good  and  the  precordial  distress 
is  mild  and  yields  to  therapy,  the  patient  may  continue  a  fairly  com- 
fortable existence  for  years ;  in  such  cases,  fair  but  somewhat  guarded 
prognoses  regarding  longevity  may  be  given.  Widespread  coronary 
disease  may  show  itself  clinically  in  several  ways :  by  severe  attacks 
of  precordial  distress  (angina  pectoris),  in  any  of  which  the  patient  may 
die  from  edema  of  the  lungs,  coronary  infarct,  or  embolus ;  by  attacks 
of  dyspnoea ;  by  vomiting  which  has  no  relation  to  the  ingestion  of  food 
and  is  often  ascribed  to  indigestion  and  hyperacidity ;  or  by  slight 
febrile  disturbances  combined  with  tender  areas  over  the  precordium. 
I  believe  the  latter  is  sometimes  due  to  focal  myocardial  or  even  to  myo- 
malaceous  areas  from  an  infective  or  embolic  process  in  a  secondary 
coronary  vessel.  Such  a  process  may  run  its  course  in  a  few  days  or 
weeks ;  the  heart  becomes  permanently  affected,  but  the  damage  is 
not  necessarily  incompatible  with  life  or  with  a  fair  amount  of  comfort. 
The  prognosis  depends  upon  the  severity  of  the  infection  as  judged  by 
the  temperature,  rigors,  duration,  and,  especially,  by  the  frequency  of  the 
attacks.  When  the  clinical  manifestations  are  mild,  with  only  occasional 
recurrences,  the  prognosis  is  fair,  for  the  chances  are  that  the  myocar- 
dial damage  occurring  with  each  infection  will  only  gradually  cripple  the 
heart,  and  that  symptoms  of  myocardial  insufficiency  will  supervene 
only  after  a  long  period  of  time.  The  chief  danger  is  the  possibility  of 
embolic  infarcts  into  some  vital  organ ;  for  example,  the  brain. 

The  main  right  or  left  coronary  artery  may  be  suddenly  plugged  by  an 
embolus,  or  its  lumen  closed  by  an  infarct.  This  is  usually  accompanied 
by  intense  precordial  distress,  dyspnoea,  and  gastric  symptoms.  Signs  of 
acute  cardiac  failure  rapidly  supervene,  and  death  usually  occurs  within 
24  hours.     Such  cases  have  been  corroborated  by  necropsy  examinations. 

Ventricular  fibrillation  is  probably  another  type  of  sudden  death  oc- 
curring in  patients  with  cardiosclerosis.  As  far  as  our  knowledge  goes, 
this  arrhythmia  is  apparently  almost  immediately  fatal.1  At  present 
there  is  no  method  by  which  its  advent  can  be  foretold.  It  seems  most 
likely  to  occur  in  patients  who  receive  digitalis  (Chapter  XVI)  and  who, 
just  preceding  the  presumed  fibrillation  attack,  are  in  a  fair  state  of 
compensation  and  apparently  progressing  favorably. 

The  degree  of  cardiac  hypertrophy  has  a  certain  influence  in  increas- 
ing the  probability  of  'acute  accidents,'  especially  after  a  first  attack 

1  Robinson,  however,  recently  reported  a  case  in  which  the  patient  lived  sev- 
eral weeks  after  the  onset  of  ventricular  fibrillation. 


204  CLINICAL  CARDIOLOGY 

of  decompensation.  The  cardiac  reserve  power  is  then  apt  to  be  quickly 
exhausted,  even  after  the  restoration  of  compensation.  This  may 
evince  itself  by  the  presence  of  dyspnoea,  slight  edema,  visceral  con- 
gestion, or  by  arrhythmias,  especially  extrasystoles.  The  usual  agonal 
stages  consist  in  edema  of  the  lungs  coming  on  in  attacks,  or  in  steadily 
increasing  pulmonary  engorgement. 

Prognostically  hypertension  forms  an  extremely  important  factor  in 
the  possible  causation  of  cerebral  hemorrhage.  There  is,  however,  no 
definite  method  of  foretelling  these  apoplectic  attacks.  In  many  cases 
the  blood  pressure  is  high  for  months  or  years,  and  cerebral  hemorrhage 
does  not  supervene ;  in  others,  hypertension  is  only  moderate  and  hem- 
orrhage does  occur.  The  reason  for  this  probably  lies  in  the  fact  that 
this  accident  depends  not  only  upon  the  degree  of  hypertension  but  also 
upon  the  extent  of  the  cerebral  arteriosclerosis.  In  the  absence  of  brain 
symptoms,  we  possess  no  means  of  determining  the  extent  of  cerebral 
arteriolar  disease. 

Uremia  is  another  frequent  form  of  death  in  cardiosclerosis.  It  has 
been  found  that  the  diastolic  pressure  is  of  great  significance  in  deter- 
mining the  probability  of  uremic  complications.  A  diastolic  pressure 
of  110  mm.  or  over  is  regarded  as  a  danger  signal;  the  higher  the 
diastolic,  the  greater  the  chances  for  uremia,  with  all  its  symptoms  and 
complications.  Briefly,  these  are  vomiting,  nausea,  headache,  oli- 
guria, dyspnoea,  and  pallor.  The  special  prognostic  features  of  each 
of  these  manifestations  are  beyond  the  scope  of  our  subject. 

Physical  Signs  of  Ventricular  Hypertrophy 

The  possibility  of  correctly  diagnosing  cardiac  hypertrophy  by  the 
usual  physical  signs  depends  chiefly  upon  the  extent  of  the  hypertrophy 
and  the  thickness  of  the  chest  wall.  For  example,  the  tremendous 
impact  to  the  thoracic  wall  in  the  far  advanced  and  extreme  ventricular 
hypertrophy  of  typical  aortic  insufficiency  can  scarcely  be  mistaken, 
for  it  produces  a  visible  and  palpable  shock  to  the  entire  left  half  of 
the  chest.  It  is  the  lesser  degrees  of  cardiac  hypertrophy  which 
especially  require  diagnostic  consideration.  Hypertrophic  and  enlarged 
hearts,  in  which  myocarditis  is  an  important  pathological  factor,  are 
often  not  diagnosed  because  the  impaired  condition  of  the  circulation 
is  such  that  the  usual  vigorous,  unhampered  action  indicative  of  hyper- 
trophy is  absent.  The  diagnosis  must  then  depend  upon  the  data  al- 
ready indicated  in  the  description  of  the  physical  signs  of  myocarditis 
(q.v.). 

When  typical,  left  ventricular  hypertrophy  produces  a  booming, 
loud,  first  sound  over  the  entire  cardiac  area,  and  a  broad,  heaving  sys- 
tolic impact  distinctly  palpable  well  outside  the  normal  cardiac  limits. 
It  must  be  remembered,  however,  that  these  characteristics  may  be 
simulated  in  thin-chested  individuals  in  whom  the  heart  is  well  applied 


MYOCARDITIS  AND   CARDIOSCLEROSIS  205 

to  the  chest  wall,  or  by  hearts  in  which  the  systolic  action  is  violent 
(for  example,  in  exophthalmic  goiter).  Such  instances  demonstrate 
the  necessity  for  reserve  in  the  diagnosis  of  ventricular  hypertrophy, 
particularly  in  view  of  the  fact,  already  pointed  out,  that  it  is  extremely 
difficult  to  delimit,  even  approximately  by  percussion,  the  size  of  the 
cardiac  area.  In  other  words,  the  physical  evidence  of  cardiac  enlarge- 
ment must  be  definite  and  unmistakable  before  its  diagnosis  is  ventured. 
An  accentuated  second  sound  at  the  apex  or  at  the  second  right  inter- 
space is  sometimes  accepted  as  an  indication  of  left  ventricular  hyper- 
trophy. It  is  true  that  these  abnormally  accentuated  sounds  are  then 
often  present,  but  they  must  be  regarded  not  as  evidence  of  hyper- 
trophy, but  rather  of  hypertension  in  which  left  ventricular  hypertrophy 
is  often,  but  not  invariably,  present.  A  reduplicated  apical  impulse 
(gallop  rhythm)  is  sometimes  present  in  the  hypertensive  cases,  es- 
pecially when  cardiac  hypertrophy  exists. 

The  diagnosis  of  right  ventricular  hypertrophy  is  even  more  difficult 
and  problematical  than  that  of  the  left.  A  second  pulmonic  sound, 
relatively  or  actually  accentuated  when  compared  with  the  second 
aortic,  is  regarded  as  evidence  of  overstrain  of  the  right  heart,  and 
hence  indicative  of  probable  right-sided  hypertrophy.  However,  I 
have  observed  moderate  accentuation  of  the  pulmonic  second  sound 
very  frequently  in  children  and  adults  with  normal  hearts  in  whom 
tachycardia  existed.  I  believe  that  a  comparative  study  of  this  sound 
with  the  aortic  is  of  value  as  an  indication  of  probable  impairment  of 
the  right  ventricle  only  if  the  accentuation  is  pronounced  and  tachy- 
cardia is  absent.  Even  then  the  question  of  hypertrophy  must  rest  upon 
the  length  of  time  during  which  the  accentuation  has  been  observed, 
the  type  of  lesion,  and  upon  other  associated  data.  In  marked  right 
ventricular  hypertrophy  the  apex  may  be  pushed  to  the  left,  so  that 
the  anterior  surface  of  the  heart  consists  chiefly  or  entirely  of  the  right 
ventricle.  Furthermore,  the  cardiac  area  of  dullness  may  not  be  in- 
creased to  the  right  because  the  right  ventricle  normally  lies  mainly  upon 
the  diaphragm.  Marked  visible  and  palpable  epigastric  pulsation 
and  systolic  retraction  of  the  apical  impulse  are  the  physical  signs  upon 
which  most  stress  is  laid  in  the  diagnosis  of  right  ventricular  hypertrophy. 
In  a  series  of  cases  in  which  the  ventricles  wrere  separately  weighed  at 
necropsy,  Lewis  did  not  find  either  visible  or  palpable  epigastric  pulsa- 
tion or  thrust  in  a  sufficient  percentage  of  cases  to  make  these  signs  of 
diagnostic  value.  These  are  examples  of  the  difficulties  with  which  the 
diagnosis  of  right  ventricular  hypertrophy  is  surrounded. 

It  is  thus  evident  that,  except  for  massive  ventricular  hypertrophy, 
the  clinical  diagnosis  of  left  or  right  ventricular  hypertrophy  from 
physical  signs  alone  is  often  problematical,  and  that  in  many  instances 
its  presence  can  only  be  correctly  inferred  in  conjunction  with  the 
known  pathological  lesion,  —  valvular,   myocardial,  or  nephritic. 


CHAPTER  XVI 
THERAPY  IN   CIRCULATORY  DISEASE 

The  list  of  drugs  used  in  cardiovascular  disease  includes  some  which, 
upon  careful  clinical  and  pharmacological  investigation,  have  been 
found  of  no  or  only  problematical  value.  Those  of  known  value  only 
will  be  here  described. 

Digitalis 

Digitalis  or  foxglove  had  been  used  empirically  for  very  many  years, 
Our  knowledge  of  its  action  has  been  recently  enhanced  by  the  use  of 
graphic  tracings.  There  still  exists  some  difference  of  opinion  as  to  the 
method  of  its  action.  According  to  the  most  reliable  clinical  and  ex- 
perimental data,  the  latter  may  be  divided  into  two  chief  components : 
the  effect  upon  the  cardiac  contractile  power  and  that  upon  the 
mechanism  controlling  cardiac  rhythm.  Digitalis  increases  the  con- 
tractile power,  the  pumping  or  driving  force  of  the  heart;  there  is 
good  ground  for  the  assumption  that  this  is  due  to  direct  action  upon  the 
cardiac  musculature. 

Action  of  Digitalis  in  Arrhythmias.  —  The  drug  often  influences 
the  irregular  ventricular  action  commonly  met  in  auricular  fibrillation ; 
this  seems  due  to  an  effect  upon  the  auriculo-ventricular  junctional 
tissue  whereby  many  of  the  discordant  auricular  impulses  are  blocked. 
As  a  result,  ventricular  action  becomes  steadier,  slower,  and  more 
regular,  changes  which  are  indicated  by  the  pulse.  On  the  other  hand, 
digitalis  can  induce  arrhythmias  of  almost  all  types  in  rhythmically 
beating  hearts.  Most  common  of  these  are  sinus  arrhythmia,  ven- 
tricular extrasy stoles  (especially  coupled  rhythm).  Delayed  conduction 
time,  blocked  auricular  beats,  heart  block,  alternation,  and  auricular 
fibrillation  are  also  occasionally  observed.  Thus  the  double  effect  of 
digitalis  —  its  use  in,  and  its  production  of,  arrhythmias  —  has  caused 
confusion  in  the  therapeutic  indication  of  the  drug.  This  confusion 
becomes  less  when  it  is  understood  that  digitalis  arrhythmias  are 
most  probably  of  neurogenic  origin.  One  evidence  of  this  is  the  fact 
that  they  usually  disappear  upon  subcutaneous  injections  of  atropine 
sulphate.     Another  is   that  at  least  two  types  of  digitalis  arrhythmia 

206 


THERAPY   IN   CIRCULATORY  DISEASE  207 

—  sinus  arrhythmia  and  sino-auricular  block  —  are  known  to  be  due 
to  vagus  excitation.  Some  patients  are  hypersensitive  to  the  neuro- 
tropic action  of  the  drug  and  very  soon  develop  cardiac  irregularities. 
Thus,  a  young  man  of  23,  with  a  typical  rheumatic  mitral  regurgitant 
lesion,  entered  the  hospital  with  the  usual  signs  of  decompensation.  His 
pulse  was  regular.  Several  courses  of  digitalis  were  required  to  restore 
compensation.  Each  time,  the  beneficial  effects  of  the  drug  were 
coincident  with  the  inception  of  auricular  fibrillation  and  coupled 
rhythm.  After  digitalis  had  been  discontinued  for  a  few  days  the 
pulse  again  became  rhythmical.  Of  added  interest  is  the  fact  that  the 
patient  complained  of  such  extreme  hunger  and  hunger  pangs  with 
the  fibrillation  attacks  that  he  could  not  rest  unless  frequently  fed  dur- 
ing the  night.  In  another  connection,  I  have  pointed  out  that  such 
symptoms  are  probably  due  to  vagus  excitation.  This  is  of  practical 
importance  because  the  advent  of  these  peculiar  symptoms  is  a 
warning  that  sufficient  digitalis  has  been  given.  Such  manifestations 
must  be  differentiated  from  the  nausea  and  vomiting  common  in 
digitalis  poisoning.  Hunger  and  hunger  pangs  precede  the  usual 
vomiting  by  two  or  three  days ;  hence  vomiting  can  be  avoided  by 
discontinuing  medication  in  those  rare  instances  in  which  hunger 
symptoms  follow  the  administration  of  digitalis. 

When  extrasystoles  are  present  and  not  associated  with  cardiovascular 
disease,  the  drug  is  not  indicated,  although  occasionally  so  employed  on 
account  of  its  power  to  increase  vagus  inhibition.  When  extrasystoles 
accompany  cardiac  failure,  they  often  depend  upon  some  profound 
nutritional  disturbance  of  the  cardiac  musculature.  Digitalis  is  then 
definitely  indicated ;  for,  with  restoration  of  compensation,  extrasystoles 
disappear.  This  action  may  depend  upon  direct  improvement  of  the 
intracardiac  circulation  with  consequent  improvement  of  cardiac 
nutrition.  In  auricular  flutter,  digitalis  is  employed  with  a  double 
object :  to  benefit  the  cardiac  failure  which  is  usually  present,  and  to 
attempt  to  change  flutter  to  auricular  fibrillation.  When  the  latter  is 
accomplished,  the  drug  is  stopped ;  normal  rhythm  is  then  often 
resumed.  Many  instances  of  the  final  change  of  flutter  to  sequential 
rhythm  after  the  use  of  digitalis  have  been  described.  However,  I 
have  observed  one  case  of  auricular  flutter  accompanying  acute 
rheumatic  endocarditis  without  decompensation,  in  which  the  drug 
did  not  have  this  effect.  The  flutter  appeared  and  disappeared  several 
times  pari  passu  with  the  febrile  rheumatic  manifestations.  It  finally 
remained  absent  with  the  subsidence  of  the  rheumatism.  One  year 
later  the  pulse  was  still  rhythmical.  In  other  words,  digitalis  in 
large  doses  had  no  effect  upon  the  arrhythmia  nor  upon  the  restoration 
of  the  normal  rhythm.  This  negative  result  might  have  been  antici- 
pated, for  the  effect  of  digitalis  in  changing  auricular  flutter  to  normal 
rhythm  probably  depends  chiefly  upon  the  relief  of  decompensation, 
a  marked  feature  in  most  cases  of  flutter. 


208  CLINICAL  CARDIOLOGY 

If  cardiac  failure  exists,  complete  heart  block  in  itself  is  not,  I  believe, 
a  contraindication  to  the  use  of  digitalis,  for  the  drug  cannot  increase 
the  dissociation  already  present.  As  an  instance :  I  reported  a  case  of 
complete  heart  block  in  which  the  cause  of  the  dissociation  could  not 
be  ascertained  during  life.  Digitalis  was  administered  several  times 
until  vomiting  resulted.  There  was  no  change  in  the  dissociation,  the 
only  effect  of  the  drug  being  a  subjective  thumping  sensation  in  the 
chest.  In  incomplete  heart  block  digitalis  has  been  regarded  as  contra- 
indicated  because  of  the  danger  of  the  development  of  complete  block. 
This  conversion  has  been  reported  in  two  cases.  One  came  to  autopsy. 
Lesions  involving  the  conduction  system  and  part  of  the  sino-auricular 
node  were  found;  but  similar  pathological  changes  in  an  instance  of 
auricular  fibrillation  and  heart  block,  lasting  many  years,  have  been 
described,  and  digitalis  played  no  role  in  the  arrhythmia.  The  second 
case  was  one  of  severe  long-continued  decompensation.  Digitalis  was 
given  for  several  days ;  heart  block  and  auricular  fibrillation  occurred 
and  continued  until  death  a  few  days  later.  These  two  reports  do  not 
offer  sufficient  evidence  that  digitalis  alone  was  the  cause  of  the  block. 
In  neither  case  was  there  clinical  evidence  of  any  ill  effects  from  the 
presumed  induction  of  complete  heart  block  by  the  drug.  It  appears 
to  me  that  the  possible  danger  of  changing  an  incomplete  to  complete 
block  in  digitalis  medication  may  be  averted  by  the  judicious  admin- 
istration of  atropine.  The  latter  should  be  given  in  full  physiological 
doses,  administered  as  frequently  as  the  digitalis  but  about  one  half  an 
hour  before  it;  for  example,  atropine  may  be  given  before  and  the 
digitalis  after  meals. 

In  one  of  my  patients  with  complete  heart  block  in  whom,  through  a 
nurse's  inadvertence,  digitalis  had  been  continued  for  a  long  time, 
auricular  fibrillation  and  coupled  rhythm  were  produced  in  addition  to 
the  dissociation.  These  arrhythmias  were  not  followed  by  any  demon- 
strable change  in  the  clinical  condition. 

Pulse  alternation  is  also  occasionally  caused  by  digitalis.  Because 
of  its  usual  serious  prognostic  import  when  not  produced  by  drugs, 
digitalis  alternation  might  a  priori  be  considered  as  a  contraindication 
to  further  medication.  A  case  has  been  reported  in  which  alternation 
and  extrasystoles  were  produced  by  digitalis;  despite  this,  the  drug 
was  continued  and  the  patient  showed  gradual  improvement.  The 
underlying  cause  of  alternation  in  cardiac  failure  is  not  known.  When 
produced  by  digitalis,  it  apparently  is  not  dangerous,  and  in  itself  does 
not  warrant  discontinuance  of  the  drug. 

As  already  indicated,  the  contradictory  effects  of  digitalis  are  ex- 
plicable upon  the  basis  of  its  two  distinct  actions :  that  upon  the 
neurogenic  control  of  the  heart,  thus  affecting  the  rhythm;  and  that 
upon  the  contractile  power.  Although  these  effects  are  usually  coin- 
cident, the  former  may  precede  the  latter  by  one  or  several  days.  In 
other  words,  arrhythmias  occasionally  occur  before  decompensation  is 


THERAPY  IN   CIRCULATORY  DISEASE  209 

relieved.  I  do  not  regard  such  early  appearance  of  digitalis  arrhythmias 
as  any  contraindication  to  further  medication.  The  circulation  is 
only  rarely  affected  by  these  irregularities ;  the  drug  should  be  pushed 
in  the  usual  fashion  until  the  beneficial  effects  upon  the  circulation  are 
noted.  If  then  the  drug  is  stopped,  the  arrhythmias  usually  soon  dis- 
appear. 

Digitalis  Vomiting  —  Administration  of  Atropine  with  Digitalis. 
—  Digitalis  vomiting  has  been  commonly  ascribed  to  irritation  of  the 
gastric  mucosa,  but  this  scarcely  explains  the  marked  variations  in  sus- 
ceptibility to  the  emetic  action  of  the  drug.  Some  patients  vomit 
almost  immediately,  others  only  after  massive  doses  have  been  given. 
A  very  suggestive  explanation  of  this  phenomena  is  found  in  experi- 
ments on  cats  in  whom  the  alimentary  tract  was  removed ;  none  the 
less,  all  the  accompanying  manifestations  of  emesis  occurred  when 
digitalis  bodies  were  injected  intravenously.  These  experiments 
strengthen  the  belief  that  digitalis  vomiting  is  probably  due  to  central 
nerve  action  and  not 'to  peripheral  irritation.  This  fact  is  of  prac- 
tical clinical  importance  because,  in  susceptible  patients,  small  initial 
doses  of  digitalis  may  be  advantageously  combined  with  atropine 
sulphate  in  doses  of  tfo1  of  a  grain ;  subsequently  the  digitalis  dosage 
may  be  gradually  increased  to  the  usual  maximum.  In  this  manner 
I  have  succeeded  in  administering  digitalis  to  some  patients  in  whom 
even  small  doses  ordinarily  produced  vomiting.  Details  of  the  com- 
bined administration  of  digitalis  and  atropine  are  given  in  the  following 
illustrative  cases : 

Male,  age  60,  suffered  from  chronic  bronchitis,  dyspnoea,  and  asth- 
matic attacks  for  many  years.  The  patient  was  cyanotic,  physical 
signs  of  chronic  bronchitis,  emphysema,  and  myocarditis  were  present, 
the  pulse  was  completely  irregular  (auricular  fibrillation) .  The  tincture 
of  digitalis  and  Karrell  diet  (q.v.)  were  given.  At  the  end  of  one  week 
he  was  very  much  improved ;  digitalis  was  discontinued  because  of 
vomiting.  After  two  weeks  the  drug  was  again  given  with  the  same 
result.  On  the  third  administration  it  was  combined  with  atropine 
sulphate,"  grain  two;  later  grain  rso1?  given  subcutaneously.  In  this 
manner  digitalis  was  administered  continuously  for  several  weeks 
without  inducing   vomiting  and  with  excellent  clinical  results. 

Female,  age  twenty-seven  years,  had  auricular  fibrillation,  a  double 
mitral  lesion,  and  a  decompensated  heart.  Fifteen  minims  of  tincture 
of  digitalis,  three  times  a  day,  were  prescribed.  Upon  three  occasions, 
after  three  days'  administration,  medication  was  discontinued  because 
of  nausea  and  headache.  On  two  subsequent  occasions  digitalis  was 
combined  with  atropine  sulphate;  one  fiftieth  of  a  grain  was  given 
subcutaneously  when  nausea  was  already  present  and  continued  in 
doses  of  yts  grain  three  times  a  day.  Upon  the  second  occasion,  atro- 
pine and  digitalis  were  given  uninterruptedly  for  two  weeks  without 
nausea.     Decompensation  was  relieved. 


210  CLINICAL   CARDIOLOGY 

Female,  age  twenty-six,  had  a  rheumatic  mitral  regurgitant  lesion. 
There  were  broken  compensation  and  cardiac  pains  for  several  months. 
Tincture  of  digitalis,  one  drachm  daily  in  divided  doses,  was  given. 
Usually  after  a  few  days  medication  was  discontinued  because  of 
vomiting  and  headache,  and  the  decompensation  which  had  been 
temporarily  relieved,  soon  recurred.  Caffeine,  digipuratum,  and  tincture 
of  strophanthus  were  substituted  for  the  tincture  of  digitalis  without 
effect.  Finally  the  latter  was  combined  with  atropine  sulphate,  grain 
Tiro',  given  internally,  three  times  a  day.  This  was  continued  in  two 
weekly  periods,  with  interruptions,  for  many  months,  and  the  patient 
showed  improvement.  Her  appetite  remained  good.  She  finally 
decompensated  again  and  died. 

The  preparation  and  dosage  of  digitalis  have  long  been  matters  of 
dispute.  My  preference  has  been  for  the  tincture,  or  for  an  infusion 
freshly  prepared  from  potent  leaves.  A  good  tincture  kept  in  a  properly 
stoppered  bottle  will  retain  its  strength  for  several  months.  The  ob- 
jection to  the  infusion  is  that  it  must  be  freshly  prepared  and  requires 
large  dosage,  and  is  more  unpalatable  than  the  tincture.  The  tincture 
and  infusion  are  therapeutically  alike.  I  have  also  found  the  digipura- 
tum tablet  an  excellent  and  reliable  preparation ;  it  is  standardized  in 
frog  heart  units.  One  tablet  of  one  and  one  half  grains  is  equivalent  to 
fifteen  minims  of  the  tincture.  It  sometimes  seems  more  efficacious  than 
the  tincture,  especially  when  administered  in  chronic  cardiac  disease. 

Variability  in  absorption  is  no  doubt  a  large  factor  in  variability  of 
the  action  of  digitalis  when  given  by  mouth.  Digitalis  dosage  should 
be  regulated  by  the  degree  of  cardiac  failure  and  the  type  of  cardiac 
disease.  In  general,  very  little  if  any  good  is  accomplished  by  starting 
with  doses  very  much  below  the  average.  The  usual  total  amount  of 
the  tincture  required  for  full  therapeutic  effect  varies  from  one  to  one  and 
one  half  ounces  taken  over  a  period  of  about  one  week.  The  average 
daily  amount  is  one  drachm  given  in  fifteen  or  twenty  minim  doses. 
It  is  best  administered  undiluted  because  it  has  been  found  that  the 
admixture  of  water  may  interfere  with  absorption.  If  urgency  demands 
it,  very  much  larger  initial  amounts  can  be  safely  given.  One  observer, 
for  example,  has  given  initial  doses  of  several  drachms  of  the  tincture 
with  great  benefit  and  no  untoward  symptoms  except  occasional  nausea 
and  vomiting.  In  urgent  cases  I  have  also  often  administered  the  tinc- 
ture in  drachm  doses  four  or  five  times  daily ;  no  ill  effects  were  ob- 
served. The  usual  dose  of  the  infusion  is  from  one  half  to  one  ounce 
given  three  or  four  times  daily.  This  amount  can  likewise  be  con- 
siderably increased  if  quick  effects  are  desired. 

The  therapeutic  effects  of  digitalis  in  patients  with  rhythmical 
heart  action  become  evident  by  improvement  in  the  signs  of  decom- 
pensation, especially  dyspnoea,  edema,  and  the  urine  output.  In 
auricular  fibrillation  with  a  completely  irregular  and  rapid  pulse,  the 


THERAPY  IN   CIRCULATORY  DISEASE  211 

therapeutic  action  is  shown,  in  addition,  by  the  elimination  of  the  ir- 
regular and  weaker  ventricular  contractions,  the  frustate  ventricular 
activity  which  produces  no  pulse  beats  (so-called  pulse  deficit).  In 
consequence,  ventricular  rhythm  becomes  steadier  and  slower,  and  the 
pulse  tends  to  become  correspondingly  regular.  Some  observers  advise 
discontinuance  of  the  drug  or  decrease  of  its  dosage  when  this  result 
has  been  achieved.  This  advice  should  be  followed  only  if  the  drug  had 
produced  nausea  and  vomiting,  if  decompensation  had  been  relieved, 
or  if  the  usual  amount  of  digitalis  (about  one  ounce  of  the  tincture) 
had  already  been  taken ;  for  it  occasionally  happens  that  the  typical  dis- 
cordant arrhythmia  of  auricular  fibrillation  comes  under  sudden  control 
after  a  few  doses,  while  signs  of  heart  failure  continue  or  quickly  recur 
if  digitalis  is  then  stopped.  In  other  words,  with  the  exceptions  noted, 
the  administration  of  the  drug  should  be  continued  until  decompensa- 
tion is  restored. 

Coupled  rhythm  —  an  occasional  result  of  digitalis  medication  in 
auricular  fibrillation  —  is  usually  regarded  as  a  definite  warning  to  stop 
the  drug.  In  order  to  decide  this  question  for  myself,  I  kept  several 
patients  under  the  effects  of  the  drug  for  a  varying  length  of  time  after 
coupled  rhythm  had  been  induced.  Most  of  them  were  elderly  indi- 
viduals with  cardiosclerosis.  In  each  case,  digitalis  in  moderate  doses 
was  continued  for  several  weeks  after  the  beginning  of  coupling.  The 
patients  were  allowed  to  walk  about.  They  all  felt  quite  comfortable, 
there  were  no  ill  effects.  Improvement  was  particularly  noticeable 
in  one  individual  who  was  under  treatment  for  a  second  severe  break 
in  compensation.  Besides  cardiosclerosis,  he  had  had  emphysema  with 
profuse  expectoration  for  years.  The  typical  gross  pulse  irregularity 
of  auricular  fibrillation  was  present.  Digitalis  produced  coupled 
rhythm  within  five  days.  Medication  was  continued  for  two  weeks 
longer  although  the  ventricular  rate  became  as  low  as  40  per  minute. 
Cyanosis  disappeared,  expectoration  ceased ;  the  patient  stated  that 
he  had  not  been  so  free  from  cough  and  expectoration  for  years. 
Digitalis  was  then  discontinued ;  coupled  rhythm  and  improvement 
remained  ;  the  patient  passed  from  observation  a  few  weeks  later. 

With  reference  to  auricular  fibrillation  occurring  in  cardiac  decom- 
pensation, it  remains  to  be  added  that  the  patient  must  be  kept  under 
the  influence  of  digitalis  for  months  or  years  in  order  to  retain  proper 
control  of  ventricular  action  and  pulse  rate.  In  this  manner,  indi- 
viduals can  be  kept  in  a  good  or  fair  state  of  compensation  for  many 
years.  Properly  supervised,  this  long-continued  medication  can  be 
carried  out  with  no  harmful  after-effects. 

In  decompensated  cases  with  rhythmical  pulse  and  moderate 
tachycardia,  the  latter  is  often  reduced  to  normal  rapidity  with  gradual 
restoration  of  compensation,  by  the  administration  of  digitalis.  This 
is  sometimes  brought  about  by  the  inception  of  such  digitalis  arrhythmias 
as  sinus  slowing,  sino-auricular  block,  and  blocked  auricular  beats.     As 


212  CLINICAL   CARDIOLOGY 

already  indicated,  a  moderately  slow  pulse  rate  is  in  itself  no  contra- 
indication to  the  further  administration  of  the  drug,  although  in  the  type 
under  discussion  it  is  apt  to  be  coincident  with  the  full  therapeutic 
effect. 

Older  patients  with  cardiosclerosis  and  decompensation  usually 
require  larger  and  longer-continued  digitalis  dosage  than  younger  in- 
dividuals with  cardiac  failure.  The  former  are  often  comfortable  with 
ventricular  rates  between  45  and  50 ;  if  digitalis  is  then  stopped,  edema 
of  the  lungs  occasionally  develops.  Such  elderly  individuals  should 
be  kept  under  full  digitalis  effects  by  giving  them  several  courses  of  the 
medication  over  a  series  of  weeks.  This  is  best  accomplished  by  giving 
one  ounce  of  the  tincture  (about  one  drachm  daily)  for  the  first  week ; 
it  is  then  discontinued  for  the  following  week.  In  the  third  week  about 
one  half  ounce  of  the  tincture  will  be  required.  It  should  then  be 
again  discontinued  for  a  week.  In  the  succeeding  weeks  somewhat 
smaller  doses  are  adequate.  In  this  manner,  the  heart  can  be  safely 
saturated  with  digitalis  and  the  patient  kept  under  its  influence  for  a 
long  time. 

Much  has  been  written  about  the  cumulative  effect  of  digitalis  and 
the  dangers  therefrom.  Variability  in  gastric  absorption  may  be  one 
of  its  main  causes.  Unless  the  usual  mild  toxic  symptoms  are  meant 
(headache,  nausea,  arrhythmias),  digitalis  cumulation  is  a  very  infre- 
quent phenomenon,  and  its  dangers  have  undoubtedly  been  exaggerated. 
Digitalis  has  been  administered  in  innumerable  instances  for  weeks  and 
months,  and  even  years,  with  no  dangerous  effects.  In  only  one  in- 
stance did  I  observe  symptoms  which  might  be  interpreted  as  due  to 
a  cumulative  effect.  A  woman  of  40  with  a  double  mitral  lesion,  or- 
thopncea,  anasarca,  cyanosis,  and  typical  auricular  fibrillation  entered 
the  hospital  in  extremis.  Infusion  of  digitalis  in  one  half  ounce  doses 
was  given  every  four  hours.  After  three  ounces  had  been  taken  the 
patient's  condition  was  improved.  Suddenly  vomiting,  a  sudden  drop 
of  ventricular  rate  to  60,  and  cold  face  and  extremities  developed. 
Hypodermic  injections  of  strychnine  and  caffeine  had  no  effect  upon 
this  condition.  Despite  these  apparently  alarming  symptoms,  the 
patient  felt  quite  comfortable,  orthopncea  temporarily  disappeared, 
cyanosis  decreased,  and  the  urinary  output  markedly  increased.  The 
patient  died  two  days  later  from  cardiac  failure. 

The  duration  of  the  action  of  digitalis  after  its  discontinuance  is 
not  definitely  known.  From  electrocardiographic  changes  sometimes 
produced  by  digitalis  (Chapter  VI),  it  would  seem  that  after  full  thera- 
peutic doses  have  been  given,  the  effects  are  continued  for  some  weeks. 
This  substantiates  the  clinical  observation  that  after  thorough  digitali- 
zation,  the  effects  of  the  drug  are  maintained  by  giving  much  smaller 
doses. 

It  is  conceivable  that  there  is  one  possible  danger  in  administering 
digitalis  in  unnecessarily  large  doses  over  long  periods ;  i.e.  the  produc- 


THERAPY   IN   CIRCULATORY  DISEASE  213 

tion  of  ventricular  fibrillation,  an  arrhythmia,  which,  so  far  as  we  now 
know,  is  universally  fatal.  We  possess  neither  experimental  nor  clinical 
grounds  for  this  assumption.  I  predicate  it  upon  the  power  of  digitalis 
to  incite  all  types  of  cardiac  irregularities,  and  upon  the  occasional 
clinical  observation  that  patients  who  were  apparently  improving 
under  full  digitalis  dosage  sometimes  die  quite  suddenly,  and  no  reason 
for  the  sudden  fatal  termination  can  be  found  at  autopsy.  Some  of 
these  deaths  have  been  assumed  to  be  due  to  ventricular  fibrillation. 

The  Use  of  Digitalis  in  Valvular  Lesions.  —  Dogmatic  distinctions 
were  formerly  made  regarding  the  various  types  of  valvular  lesions  in 
which  digitalis  was  indicated  or  contraindicated.  Abundant  clinical  ex- 
perience has  shown  that,  although  not  followed  by  equally  good  results, 
digitalis  may  be  given  in  all  forms  of  cardiac  failure,  regardless  of  the 
valve  affected.  In  general,  in  rhythmically  beating  hearts  digitalis 
is  not  followed  by  the  same  rapidly  beneficial  effects  as  in  auricular 
fibrillation.  Its  chief  value  in  the  former  lies  in  the  reduction  of  the 
cardiac  rate,  in  lengthening  the  diastole,  and  in  strengthening  ventric- 
ular contractions.  In  aortic  lesions  with  decomposition  and  left  ven- 
tricular hypertrophy,  digitalis  is  not  as  beneficial  as  in  mitral  lesions. 
This  may  depend  upon  several  factors :  except  in  the  final  stages 
of  decompensation,  there  is  less  systemic  congestion  and  edema ;  the 
cardiac  rate  is  very  susceptible  to  neurogenic  and  other  influences  which 
cause  tachycardia.  In  mitral  lesions,  tachycardia  is  not  as  common, 
congestion  and  edema  more  common,  and  these  are  the  conditions 
which  are  more  readily  influenced  by  digitalis.  Finally,  digitalis  may 
not  exert  its  full  action  upon  the  fibers  of  extremely  hypertrophied 
muscle. 

The  value  of  digitalis  in  cardiosclerosis  with  hypertension  and  cor- 
onary disease  has  often  been  questioned ;  indeed,  until  recently,  hyper- 
tension was  regarded  by  many  as  a  distinct  contraindication  to  digitalis. 
Careful  clinical  study  has  shown,  however,  that  digitalis  in  therapeutic 
doses  does  not  regularly  raise  the  blood  pressure ;  when  occasionally 
increased,  the  increase  bears  no  relation  to  the  time  of  administration 
or  dosage  of  the  drug.  I  have  treated  patients  with  hypertensive  dis- 
ease, many  of  whom  had  a  systolic  blood  pressure  of  over  200  mm.  of 
mercury,  and  I  have  never  observed  any  pressure  increment  which  could 
in  any  way  be  correlated  with  digitalis  administration.  In  fact,  in  those 
in  whom  cyanosis  and  dyspnoea  were  the  chief  manifestations,  and  in 
whom  digitalis  gave  relief,  the  blood  pressure  was  often  lowered.  This 
may  be  because  cyanosis  itself  acts  as  an  excitant  to  the  vasomotor 
center  and  thus  raises  blood  pressure  (Chapter  XIX).  This  disturbing 
factor  is  eliminated  by  the  beneficial  effect  of  digitalis  upon  the  general 
circulation. 

Another  important  consideration  in  digitalis  therapy  is  the  question 
of  its  use  in  endocarditis  and  pericarditis  during  the  acute  stages.  When 
the  heart  rate  is  increased  as  the  result  of  these  acute  inflammatory 


214  CLINICAL   CARDIOLOGY 

processes,  digitalis  has  no  effect  in  diminishing  the  pulse  rate.  This  is 
also  true  of  other  febrile  diseases,  such  as  pneumonia,  grippe,  etc.  Hence 
the  use  of  digitalis  for  the  persistent  tachycardia  of  inflammatory  con- 
ditions is  very  apt  to  be  followed  by  disappointing  results. 

In  this  connection,  I  wish  to  point  out  a  reason  for  the  futility  of 
digitalis  in  chronic  pericarditis  with  dense  and  extensive  adhesions. 
The  latter  act  mechanically,  like  a  vise,  hindering  normal  systole  and 
diastole.  I  observed  one  instance  in  an  adult  who  had  rheumatic 
arthritis  and  irregular  temperatures  for  several  weeks.  Auricular 
fibrillation  was  present.  The  obscure  physical  signs  —  a  scarcely 
audible  or  palpable  apex  beat  —  pointed  to  myocarditis  as  the  probable 
cardiac  lesion.  A  roentgenogram  of  the  chest  showed  a  somewhat 
enlarged  cardiac  shadow.  Digitalis  was  given  for  several  weeks  with 
no  effect  upon  the  slowly  increasing  heart  failure  or  upon  the  fibrillation. 
At  necropsy,  the  valves  were  normal,  the  myocardium  not  extensively 
diseased,  there  was  a  tightly  adherent  pericardium  that  encircled  and 
fixed  the  entire  heart.  In  another  instance,  a  case  of  polyserositis  of 
unknown  origin  in  a  young  male  with  dyspnoea  and  cyanosis,  X-ray 
plates  showed  definite,  sharply  defined  calcareous  plaques  in  the  peri- 
cardium. Auricular  fibrillation  with  a  fairly  regular  and  slow  ventric- 
ular rate  was  present.  The  cardiac  impulse  and  sounds  were  weak. 
Here,  also,  it  seemed  probable  that  the  vise-like  action  of  an  adherent 
and  thickened  pericardium  was  an  important  etiological  factor  in  the 
cardiac  failure  and  cyanosis.  Digitalis  had  no  influence  upon  the 
symptoms  or  arrhythmia. 

Speaking  broadly,  in  decompensated  valvular  and  cardiovascular 
disease  in  which  infection  is  either  quiescent  or  non-existent,  I  have 
found  the  following  classification  of  value  from  the  viewpoint  of  the 
probable  effect  of  digitalis  medication : 

1.  Mitral  lesions  with  rhythmic  hearts:  Improvement  only  slowly 
or  sometimes  not  at  all  upon  digitalis.  Rest  is  apparently  the  largest 
factor  in  the  improvement. 

2.  Mitral  lesions  with  auricular  fibrillation :  Unless  decompensation 
is  extreme  or  long  continued,  improvement  very  rapid  under  digitalis. 
The  irregular  cardiac  activity  is  quickly  controlled,  and,  with  it,  de- 
compensation is  usually  promptly  relieved. 

3.  Aortic  lesions  with  slight  or  moderate  ventricular  hypertrophy : 
The  drug  is  not  of  much  value,  rest  is  the  important  factor. 

4.  Aortic  lesions  with  extreme  ventricular  hypertrophy :  Reaction 
to  digitalis  not  good,  possibly  because  there  is  not  sufficient  healthy 
cardiac  muscle  upon  which  the  drug  can  act.  Even  if  auricular  fibrilla- 
tion is  present,  digitalis  is  not  apt  to  be  followed  by  beneficial  results. 

5.  Cardiosclerosis  with  decompensation :  Those  with  cardiac  failure 
and  edema,  with  or  without  hypertension,  are  apt  to  react  well  to  the 
Karrell  diet  (q.v.),  and  digitalis  and  theobromine  sodium  salicylate 
administered  on  alternate  days.     In  cardiosclerosis  and  hypertension 


THERAPY  IN   CIRCULATORY  DISEASE  215 

with  uremia  and  no  edema,  digitalis  has  very  little  effect  in  the  relief 
of  decompensation. 

Summing  up  the  effects  of  digitalis  medication,  the  following  con- 
clusions are  warranted : 

1.  The  best  single  criterion  of  the  amount  and  duration  of  digitalis 
administration  is  its  clinical  effect. 

2.  The  beneficial  effect  of  digitalis  depends  chiefly  upon  producing 
increased  contractile  power  of  the  cardiac  musculature. 

3.  The  gradual  production  of  arrhythmias  is  usually  coincident  with 
full  clinical  effects. 

4.  If  decompensation  demands  the  continuance  of  digitalis,  the 
rapid  onset  of  arrhythmias  does  not  contraindicate  its  further  use. 

5.  Atropine  sulphate,  grain  y^  to  yinr,  three  times  a  day,  given 
internally  or  subcutaneously  at  the  beginning  of  medication,  occasion- 
ally prevents  nausea  and  vomiting  in  susceptible  individuals. 

6.  The  hypertension  of  cardiovascular  disease  does  not  contra- 
indicate the  use  of  digitalis. 

7.  To  derive  clinical  benefits  quickly,  digitalis  should  be  given  in 
full  therapeutic  doses. 

8.  When  digitalis  acts  promptly  in  small  doses,  the  effect  is  likely 
to  be  temporary.  For  permanent  improvement,  long-continued  medica- 
tion is  usually  required. 

9.  Digitalis  occasionally  produces  epigastric  sensitiveness  and  hun- 
ger pangs,  which  appear  to  be  due  to  heightened  vagal  tone.  These 
symptoms  precede  vomiting  by  one  or  two  days,  and  indicate  a  full 
therapeutic  digitalis  effect. 

Tincture  Strophanthus 

This  possesses  no  advantages  over  the  tincture  of  digitalis.  Its  dis- 
advantage is  that  it  varies  considerably  in  strength.  It  should  be 
given  hi  one  half  or  one  drachm  doses,  and  not  in  the  smaller  quantities 
usually  recommended. 

Crystalline,  strophanthin  (Thorns)  is  a  most  powerful  glucoside. 
The  best  preparation  is  that  put  up  in  ampoules  containing  1  c.c.  of 
a  1  per  cent  solution.  The  dose  is  from  10  to  15  minims ;  this  should 
be  slowly  injected,  preferably  intravenously.  It  is  of  remarkable  effi- 
cacy, particularly  in  the  acute  heart  failure  of  auricular  fibrillation. 
Within  a  very  short  time,  sometimes  after  one  hour,  the  injection  may 
be  followed  by  slower  and  more  regular  ventricular  activity,  with  a 
correspondingly  good  effect  upon  dyspnoea  and  cyanosis;  frustrate 
beats  may  quickly  disappear,  edema  show  some  evidence  of  clearing 
up,  and  diuresis  increase.  If  the  urgency  of  the  case  demands  it,  the 
injection  should  be  repeated  at  the  end  of  24  hours.  In  other  words, 
these  injections  can  in  a  remarkably  short  time  produce  the  effect 
which  only  occurs  after  several  days  of  the  usual  method  of  digitalis 


216  CLINICAL  CARDIOLOGY 

administration.  On  the  other  hand,  the  effect  is  more  evanescent; 
hence,  in  the  decompensation  of  cardiac  disease,  it  is  necessary  to  follow 
up  these  injections  by  digitalis  given  in  the  usual  manner.  Strophanthin 
is  also  indicated  in  acute  cardiac  failure  from  cardiorenal  disease,  es- 
pecially if  pulmonary  edema  is  present.  There  is  one  caution  necessary 
respecting  strophanthin;  namely,  it  is  contraindicated,  or  should  be 
used  very  sparingly  if  the  patient  is  already  digitalized,  otherwise  very 
serious  toxic  symptoms  may  immediately  follow.  For  example,  in  a 
patient  with  mitral  regurgitation,  extreme  decompensation,  and  rhyth- 
mical pulse,  who  had  long  been  under  the  full  effects  of  digitalis,  this 
precaution  was  not  heeded ;  an  injection  of  1  c.c.  of  strophanthin  was 
immediately  followed  by  auricular  fibrillation,  a  condition  which  lasted 
until  death  a  few  days  later  and  undoubtedly  hastened  the  fatal  ter- 
mination. 

Tincture  of  Squills 

In  doses  of  15  to  30  minims  this  has  an  action  on  the  circulation 
similar  to  digitalis.  Like  the  latter,  it  may  produce  sinus  arrhythmia 
and  heart  block,  apparently  by  increased  vagal  inhibition.  It  possesses 
no  advantages  over  digitalis,  and  is,  in  addition,  irregular  and  un- 
certain in  action.     Squills  is  often  prescribed  in  pill  form  as  a  diuretic. 

Apocynum 

Apocynum  or  Canadian  Hemp,  given  in  fluid  or  solid  extract,  has 
been  studied  to  a  slight  extent ;  it  has  no  regular  or  marked  effect  upon 
the  circulation. 

Caffeine  and  Its  Derivatives 

Caffeine  produces  vaso-constriction  by  its  action  upon  the  vasomotor 
center;  it  also  has  a  slight  effect  upon  the  heart  itself.  Its  main 
therapeutic  value  rests  upon  the  action  on  the  kidneys.  Since  cardio- 
vascular disease  involves  the  kidneys,  a  discussion  of  caffeine  and 
its  derivatives  is  of  importance. 

Caffeine  acts  primarily  as  a  diuretic,  thereby  increasing  the  output 
of  urine.  The  manner  of  its  action  is  still  in  dispute ;  some  ascribe  it 
to  an  irritating  effect  upon  the  renal  epithelium,  others  to  an  effect 
upon  the  renal  circulation.  Caffeine  increases  principally  the  watery 
constituent  of  the  urine;  there  is  also  an  increased  output  of  solids, 
especially  of  sodium  chloride,  and,  to  a  lesser  degree,  of  the  nitrogenous 
constituents. 

The  best  method  of  caffeine  administration  is  in  the  form  of  caf- 
feine sodium  salicylate,  a  readily  soluble  salt.  A  20  per  cent  solution  of 
this  salt  in  distilled  water  lends  itself  admirably  to  hypodermic  admin- 
istration ;  the  dose  is  from  15  to  30  minims. 

Theobromine  Sodium  Salicylate.  —  This  salt  produces  more  marked 
diuresis  than  caffeine.     Another  advantage  is  that  it  has  no  effect  upon 


THERAPY  IN   CIRCULATORY  DISEASE  217 

the  vasomotor  center,  and  hence  does  not  produce  blood  pressure  changes. 
The  drug  is  administered  in  7  to  3  5  grain  (0.5  to  1  gm.)  doses  three  or 
four  times  daily,  well  diluted  in  water.  Because  of  an  unpleasant  taste, 
it  can  be  given  in  wafers.  If  the  medication  upsets  the  stomach,  it 
may  be  given  in  smaller  doses  more  frequently.  It  can  also  be  admin- 
istered per  rectum  by  the  Murphy  drip  method.  Finally,  it  can  be 
given  intravenously  according  to  a  method  which  I  have  developed. 

This  intravenous  method  seems  of  importance  because  the  drug  is 
particularly  indicated  in  uremic  conditions  with  vomiting,  delirium, 
and  disturbances  of  the  sensorium,  in  which  theobromine  cannot  be 
given  by  mouth,  or  if  so  given,  the  amount  absorbed  is  very  slight  or 
nil.  At  first  I  employed  a  solution  of  ten  grains  dissolved  in  200  c.c. 
of  water,  once  or  twice  a  day.  This  method  was  discarded  because 
it  was  too  cumbersome  and  did  not  permit  sufficiently  frequent  admin- 
istration. Now  I  use  5  per  cent  solutions,  the  percentage  ordinarily 
used  in  animal  experimentation.  Pharmacological  examinations  show 
that  the  specific  gravity  of  a  5  per  cent  solution  at  20°  C.  is  1.0228, 
and  its  alkalinity  equivalent  to  that  of  a  2.4  per  cent  solution  of  sodium 
bicarbonate.  Sodium  bicarbonate  in  this  concentration,  or  even 
stronger,  is  sometimes  given  intravenously  in  diabetic  coma.  A  5  per 
cent  theobromine  sodium  salicylate  solution  heated  in  a  closed  vessel  at 
96°  C.  for  one  hour,  again  for  one  hour,  and  then  for  one  half  hour, 
shows  slight  yellowish  discoloration  and  a  very  slight  loss  of  alkalinity, 
but  remains  perfectly  clear.  Sterilization  does  not  alter  the  solution. 
The  dose  I  usually  employ  is  15  grains,  i.e.  20  c.c.  of  the  5  per  cent 
solution.  In  one  instance  30  grains  (40  c.c.  of  the  solution)  were 
given  in  a  single  dose.  The  stock  solution  should  be  resterilized  by 
boiling  immediately  preceding  injections.  If  the  entire  solution  enters 
the  vein,  there  is  no  local  reaction.  If  a  few  drops  find  their  way  into 
the  subcutaneous  tissue,  some  induration,  ecchymosis,  or  slight  pain 
lasting  a  few  days  sometimes  follows.  In  one  instance,  through  a  mis- 
understanding by  one  of  the  house  staff,  the  solution  was  injected  sub- 
dermally;  a  local  skin  slough  and  ulcer  resulted.  The  injections  are 
never  followed  by  systemic  reactions.  The  solution  is  readily  prepared 
and  sterilized.  While  20  c.c.  of  a  5  per  cent  solution  have  been  found 
a  convenient  standard,  the  dosage  can  be  modified  to  suit  individual 
requirements.  The  ordinary  dosage  can  be  given  intravenously  daily 
for  several  days. 

It  has  been  shown  that  the  diuretic  function  of  the  kidney  becomes 
fatigued  by  long-continued  theobromine  administration,  hence  it  is 
advisable  to  give  the  drug  in  the  customary  oral  method  in  courses  of 
two  or  three  days  with  intermissions  of  similar  periods.  Theobromine 
sodium  salicylate  (diuretin)  is  particularly  indicated  in  the  dropsy  of 
cardiorenal  disease.  Given  on  alternate  days  with  digitalis,  it  often 
enhances  the  action  of  the  latter,  not  only  in  cardiorenal  but  also  in 
purely  valvular  disease.     As  an  adjuvant,  theobromine  is  often  combined 


218  CLINICAL   CARDIOLOGY 

with  the  Karrell  diet.  Because  of  its  importance,  this  diet  and  the 
method  of  its  administration  require  detailed  description. 

The  Karrell  diet  consists  in  a  daily  diet  of  800  to  1000  c.c.  of  milk ;  it 
is  preferably  given  in  glassfuls  of  six  ounces  every  three  hours.  This  is 
usually  termed  a  "  Karrell  day."  On  Karrell  days  the  patient  should 
be  in  bed  or  at  rest.  The  milk  should  be  sipped  slowly.  Patients 
rarely  complain  of  thirst,  but  occasionally  become  so  hungry  that  they 
suffer  from  hunger  pangs  and  faintness.  Under  these  conditions,  I 
allow  them  dry  toast,  crackers,  perhaps  also  an  apple  or  orange  in 
amounts  just  sufficient  to  curb  extreme  hunger.  An  excellent  routine 
procedure  in  moderately  severe  edema  of  cardiorenal  origin  is  Karrell 
diet  and  theobromine  sodium  salicylate  for  two  days,  alternating  with 
digitalis  and  an  appropriate  renal  diet  (q.v.)  with  somewhat  restricted 
fluid  intake  for  the  succeeding  two  days.  In  most  cases  I  believe  it 
advisable  to  continue  theobromine  therapy  and  Karrell  diet,  at  intervals, 
long  after  edema  has  disappeared  and  the  patient  feels  well.  These 
intervals  should  be  gradually  lengthened ;  for  example,  Karrell  diet 
and  theobromine  may  be  given  for  a  day,  at  first  twice  weekly,  then  once 
weekly,  then  once  monthly.  In  this  manner  it  seems  possible  to  retain 
and  continue  for  months,  and  occasionally  for  years,  the  improvement 
gained  by  the  initial,  more  intense  therapy.  In  some  instances  of 
cardiorenal  disease  with  extreme  anasarca,  the  intensive  treatment 
outlined  —  digitalis,  theobromine,  and  Karrell  diet  —  yields  remarkable 
results :  losses  of  from  10  to  15  pounds  during  the  first  week,  and  from 
20  to  40  pounds  in  several  weeks,  are  not  exceptional.  Coincident 
with  reduction  of  edema,  other  serious  symptoms  such  as  semistupor, 
dyspnoea,  cyanosis,  and  manifestations  of  hypertension,  often  improve 
or  disappear.  Beneficial  results  derived  from  this  therapy  are  most 
marked  in  those  in  whom  myocardial  insufficiency  is  a  prominent  clinical 
feature. 

As  a  modification  of  the  Karrell  diet  and  as  a  method  of  promoting 
diuresis  in  patients  in  whom  the  urinary  output  is  approximately 
normal  in  amount,  I  have  restricted  the  fluid  intake  to  only  500  c.c. 
daily.  The  liquids  allowed  are  water,  sweetened  or  unsweetened 
lemonade,  and  coffee  or  tea  with  very  little  milk.  When  necessary, 
only  sufficient  solids  of  the  kind  already  mentioned  are  added  to  control 
severe  hunger.  Patients  rarely  complain  of  thirst ;  when  present,  it  is 
partially  relieved  by  small  quantities  of  cracked  ice,  or  by  rinsing  the 
mouth  with  water.  I  give  this  restricted  and  modified  Karrell  diet 
for  two  days,  with  theobromine  sodium  salicylate  in  7  to  15  grain  doses 
to  the  amount  of  45  grains  daily.  Then  follow  two  days  of  digitalis 
with  appropriate  cardiorenal  diet  and  somewhat  restricted  fluid  intake. 
By  this  method,  I  have  occasionally  achieved  results  which  did  not  fol- 
low the  ordinary  Karrell  diet.  Older  patients  with  long-standing  edema 
frequently  voided  from  60  to  80  ounces,  and  occasionally  100  ounces, 
on  the  day  succeeding  the  second  theobromine  day,  the  usual  time  of 


THERAPY  IN  CIRCULATORY  DISEASE  219 

most  marked  diuretic  action.  Coincidentally,  edemas  quickly  cleared 
up,  and  cyanosis  and  especially  dyspnoea  very  rapidly  and  often  remark- 
ably improved.  These  secondary  results  may  have  been  due  not  only 
to  the  elimination  of  water,  but  also  to  elimination  of  toxic  substances. 

Strychnine 

In  animal  experiments,  strychnine  has  been  shown  to  have  a 
vaso-constrictor  influence,  and  hence  has  been  assumed  to  be  of  value 
in  low  blood  pressure  and  shock.  However,  careful  observations  of 
its  effect  on  the  circulation  in  health  and  in  cardiac  disease  have 
shown  no  influence  upon  the  urinary  output,  edema,  blood  pressure,  or 
heart  rate,  —  the  usual  criteria  of  any  change  in  the  circulation.  The 
claim,  occasionally  made,  that  in  some  intangible  way  strychnine  acts 
as  a  circulatory  'tonic'  by  its  effect  upon  the  nervous  system  is  not 
substantiated  by  any  clinical  evidence. 

Nitrites 

This  is  the  vasodilator  group.  It  consists  mainly  of  nitroglycerin, 
nitrite  of  potassium  and  sodium,  amyl  nitrite,  erythrol  tetranitrate, 
and  mannitol  hexanitrate.  Amyl  nitrite  is  the  emergency  drug  of  this 
class  and  is  considered  in  detail  in  another  section  (Chapter  XXI). 
Nitroglycerin,  the  drug  most  often  prescribed,  acts  as  a  peripheral 
arteriolar  dilator.  The  usual  dose  is  twv  grain  three  times  daily.  It 
may  be  given  hypodermically  or  by  mouth.  It  is  chiefly  used  in  circu- 
latory disease  for  lowering  blood  pressure  in  hypertension  and  for  the 
relief  of  precordial  pains.  It  is  believed  that  the  latter  is  accomplished 
by  the  relief  of  spasm  of  the  coronary  arteries.  In  some  cases  of  hyper- 
tension I  have  administered  as  much  as  tV  of  a  grain  of  nitroglycerin 
subcutaneously  three  times  daily  with  little  or  no  effect  upon  hyper- 
tension or  precordial  symptoms.  These  and  other  inconstant  results 
following  nitroglycerin  may  be  accounted  for  by  the  varying  amounts 
of  arterial  thickening  and  consequent  variations  in  the  dilating  power 
of  the  arterioles.  In  edema  of  the  lungs  with  hypertension  and  nephritis, 
nitroglycerin  in  large  doses  (from  tf  to  iV  gr.  hypodermically),  combined 
with  the  usual  cardiac  remedies,  occasionally  relieves  the  overburdened 
heart  by  its  effect  upon  the  peripheral  circulation. 

Nitroglycerin  is  of  most  value  in  cardiosclerosis  with  moderate 
hypertension  and  labile  vasomotor  mechanism  (Chapter  XXI).  Its 
administration  may  then  result  in  fairly  long-continued  lowered  blood 
pressure  and  in  relief  of  symptoms.  If  the  use  of  nitroglycerin  be  limited 
to  such  cases,  it  becomes  a  very  valuable  drug.  If,  however,  it  is  used 
in  continued  hypertension  with  advanced  coronary  disease,  nitroglycerin 
is  apt  to  be  followed  by  disappointing  results  for  reasons  already  men- 
tioned. Erythrol  tetranitrate  and  mannitol  hexanitrate  have  a  slower 
and  more  continued  action  than  the  others  of  the  vasodilator  group. 


220  CLINICAL  CARDIOLOGY 

Camphor 

This  drug,  especially  in  the  form  of  camphor  in  oil,  given  hypoder- 
mically,  has  been  a  favorite  circulatory  remedy  for  many  years.  Care- 
ful clinical  observation,  however,  has  shown  that  it  has  no  demonstrable 
influence  on  the  circulation ;  i.e.  it  exerts  no  influence  on  diuresis, 
blood  pressure,  or  pulse  rate.  In  animal  experimentation  there  is  a 
slight  effect  upon  the  pulse  pressure.  The  use  of  spirits  of  camphor 
in  depression  of  the  nervous  system,  as,  for  example,  in  fainting  spells, 
is  sometimes  of  value  because  of  its  reflex  action. 

Alcohol 

Discussion  of  alcohol  is  here  limited  to  its  effect  upon  the  circula- 
tion. In  animals,  alcohol  slightly  increases  cardiac  contractility.  In 
human  beings,  when  given  in  large  quantities,  it  produces  a  marked 
fall  of  blood  pressure  by  its  action  upon  the  vaso-constrictor  center  and 
upon  the  heart  muscle.  Small  quantities  of  alcoholic  beverages  seem 
occasionally  to  augment  cardiac  contractility  in  decompensated  cardiac 
disease,  but  the  effect  is  slight  and  inconstant,  and  its  value  prob- 
lematical. 

Aconite 

Recent  investigations  have  shown  that  the  strength  of  the  tincture 
of  aconite,  the  preparation  usually  used,  varies  considerably,  and 
that,  even  when  properly  standardized,  the  dose  ordinarily  admin- 
istered is  much  too  small.  Aconite  does  not  slow  the  heart  rate  in  cardiac 
disease.  Its  presumed  therapeutic  value  is  based  upon  experimental 
investigation  in  animals  in  which  cardiac  rate,  contractility,  and  blood 
pressure  are  lowered  as  the  result  of  a  central  vagus  effect.  When 
given  in  very  large  doses,  the  drug  sometimes  increases  ventricular  ir- 
ritability. This  has  been  shown  by  the  production  of  extrasystoles  by 
pressure  over  the  pneumogastrics  of  patients  who  had  been  given  the  drug. 

Sparteine 

This  drug  is  the  alkaloid  of  the  common  broom.  Formerly  it 
was  used  as  a  cardiac  tonic  because  it  was  presumed  to  have  an 
action  like  digitalis.  When  injected  into  animals,  it  slows  the  pulse 
and  slightly  raises  the  blood  pressure.  Clinically,  these  effects  have  not 
been  observed ;  however,  it  must  be  added  that  careful  investigation 
of  its  action  is  lacking.  The  dose  advised  ranges  from  i  to  5  grains ; 
probably  2  grains  of  sparteine  sulphate  is  a  safe  dose  for  an  adult. 

Suprarenal  Extract  —  Adrenalin 

Its  vaso-constrictor  action,  especially  when  given  intravenously,  is 
well  known.  It  may  be  used  in  circulatory  collapse  accompanied  by 
a  sharp  fall  of  the  systolic  blood  pressure,  or  in  hypertension  with 
rapidly  falling  pressure,  the  latter  indicating  myocardial  insufficiency. 
Injections  of   the  drug   in  these   conditions   are   sometimes  followed 


THERAPY  IN   CIRCULATORY  DISEASE  221 

by  decided  though  temporary  improvement.  Adrenalin  has  also  been 
advised  in  so-called  constitutional  hypotension  (Chapter  XIX),  a  con- 
dition in  which  cardiac  failure  is  absent.  The  main  symptoms  in 
these  individuals  are  those  referable  to  vasomotor  disturbances.  The 
hypotension  itself  rarely  requires  medication,  but  the  accompany- 
ing symptoms  may  be  relieved  by  adrenalin.  The  best  method  of 
administration  is  the  standard  sterile  solution  in  the  strength  of  1  to 
1000 ;  the  dose  is  from  15  to  30  minims  given  internally,  or,  preferably, 
hypodermically  or  intravenously. 

Morphine 

This  drug  produces  slowing  of  the  heart  rate  by  its  effect  upon  the 
medullary  center.  Injections  in  dogs  are  sometimes  followed  by  com- 
plete heart  block.  In  man,  morphine  is  a  cardiac  '  stimulant '  only 
in  the  sense  that,  by  its  effect  upon  the  central  nervous  system,  the 
patients  become  less  restive  and  irritable.  Thus  regarded,  it  is  often 
an  excellent  aid  to  other  drugs  in  such  acute  circulatory  conditions  as 
paroxysmal  tachycardia,  acute  onset  of  auricular  fibrillation,  and  sudden 
cardiac  failure  with  dyspnoea. 

Bromides 

These  are  indicated  in  tachycardia  from  any  cause,  or  in  those 
in  whom  extrasystoles  cause  subjective  sensations.  In  the  former, 
where  morphine  may  also  be  indicated,  the  bromides  enhance  and  pro- 
long the  morphine  effect. 

Other  sedatives  which  may  be  employed  to  combat  restlessness  and 
sleeplessness  are  chloral  hydrate  and  veronal ;  they  may  be  given  alone 
or  combined  with  small  doses  of  morphine  or  codeine. 

Acetate  of  Potash  and  Soda 

Their  diuretic  action  is  usually  slight  and  depends  upon  the  non- 
metallic  salt  —  the  acetate  —  for  its  effect.  It  is  occasionally  of 
advantage  to  alternate  these  drugs  with  the  more  active  diuretic, 
theobromine  sodium  salicylate.  The  dose  is  from  15  to  30  grains, 
given  in  solution  every  two  or  three  hours. 

Saline  Cathartics 

Brisk  catharsis  is  sometimes  of  value  in  starting  diuresis.  The  best 
saline  for  this  purpose  is  the  sulphate  of  magnesia. 

Calomel 

The  drug  is  sometimes  of  benefit  in  cardiac  dropsy ;  it  is  of  less  value 
in  edema  of  renal  origin.  The  dose  generally  recommended  is  3  grains 
three  times  daily  for  two  to  four  days ;  after  an  interval  of  a  few  days, 


222  CLINICAL   CARDIOLOGY 

unless  some  contraindication  exists,  it  may  be  repeated  in  the  same  dosage. 
Its  action  is  ascribed  to  direct  stimulation  of  the  renal  epithelium. 

Venesection 

This  procedure  has  its  sphere  in  plethoric  cases  with  cyanosis 
and  dyspnoea.  It  possesses  a  double  advantage :  temporary  decrease 
of  heart  work  by  decreasing  blood  volume,  and  removal  of  toxic 
products.  The  amount  to  be  withdrawn  must  be  individualized ;  it 
should  be  at  least  250  c.c. 

Autogenous  and  Stock  Vaccines,  and  Sensitized  Sera 

I  have  employed  autogenous  vaccines  in  a  number  of  cases  of 
endocarditis  due  to  the  streptococcus  viridans,  but  have  not  been  able 
to  discern  any  benefit  from  their  use.  There  was  no  effect  upon  the 
temperature  or  toxic  symptoms,  nor  was  there  any  change  in  the  clinical 
course  of  the  disease.  In  a  few  cases  that  came  to  necropsy  in  which 
this  therapy  was  employed,  nothing  was  found  to  indicate  that  the  vege- 
tative process  on  the  valves  was  checked  in  the  slightest  degree. 

I  have  also  administered  stock  vaccines  in  a  small  number  of  cases 
of  endocarditis  which  seemed  clinically  of  streptococcic  origin  but  in 
whom  the  organism  could  not  be  isolated  from  the  blood.  Though  I 
observed  no  ill  effects  from  the  injections,  they  had  not  the  slightest 
therapeutic  result. 

In  a  number  of  instances  of  streptococcus  viridans  infection,  I 
employed  serum  derived  from  horses  sensitized  to  this  coccus.  The 
effect  of  such  injections  was  also  entirely  negative. 

Colloidal  Silver  Preparations 

Recently,  interest  in  the  use  of  silver  salts  in  septic  conditions  has 
been  revived  by  the  administration  of  various  colloidal  silver  salts  in 
the  treatment  of  acute  rheumatic  and  bacterial  endocarditis.  I  have 
observed  a  few  cases  in  which  they  were  injected  intravenously.  In 
one,  a  streptococcus  viridans  infection,  20  injections  were  given  in  two 
or  three  day  intervals  without  benefit ;  the  patient  died  with  the  symp- 
toms of  cerebral  embolism.  In  another  instance,  a  child  with  acute 
rheumatic  endocarditis,  a  few  injections  were  followed  by  a  rather 
sharp  fall  in  temperature.  In  the  same  ward,  I  had  under  observation 
at  this  time  a  male  adult  of  20  who  suffered  from  acute  rheumatism 
and  from  acute  endocarditis  and  pericarditis  with  effusion.  The 
cardiac  involvement  ran  a  very  stormy  course :  the  temperature 
reached  105°  and  remained  between  104°  and  105°  for  one  week ; 
dyspnoea,  chiefly  due  to  the  very  large  amount  of  pericardial  exudate, 
was  extreme.  The  patient  received  neither  silver  injections  nor  serum 
therapy  of  any  kind.  After  one  week  the  temperature  fell  suddenly, 
signs  of  pericardial  effusion  quickly  disappeared,  the  patient  rapidly 


THERAPY   IN   CIRCULATORY   DISEASE  223 

convalesced  with  the  physical  signs  of  a  permanent  aortic  lesion.  Thus 
are  contrasted  two  cases  of  an  acute  endocardial  infection  both  of 
whom  rapidly  convalesced,  one  with,  the  other  without,  any  attempt 
at  specific  therapy.  The  inference  is  clear  that  there  is  no  proof  in 
the  first  case  that  the  injections  caused  a  recession  of  the  acute  endo- 
carditis. In  the  enthusiastic  reports  regarding  the  use  of  colloidal 
silver  in  endocarditis,  I  have  found  no  instance  of  '  cure  '  which 
could  not  be  explained  upon  the  basis  of  an  acute  endocarditis  which 
had  quickly  run  its  febrile  course,  or  upon  the  basis  of  a  longer  duration 
with  the  usual  remissions.  In  other  words,  I  do  not  believe  that  the 
intravenous  use  of  silver  preparations  is  warranted  in  any  type  of 
endocardial  infection. 

Massage  —  Passive  Motion 

As  a  result  of  careful  observation  of  many  cases  of  cardiac  disease, 
it  is  my  impression  that  patients  are  allowed  in  bed  or  at  absolute 
rest  too  long  after  compensation  has  been  restored,  and  after  the  in- 
flammatory process  has  run  its  course.  Two  to  three  weeks  after  the 
quiescence  of  inflammatory  symptoms  and  after  restoration  of  com- 
pensation constitute,  I  believe,  the  average  time  for  complete  rest. 
After  that  period,  the  judicious  use  of  massage,  active  and  passive 
motion,  and  exercise  aid  the  circulation  and  produce  a  more  rapid  return 
to  normal  circulatory  conditions.  No  form  of  exercise  or  massage 
should  be  pushed  far  enough  to  cause  dyspnoea,  distress,  rapid  heart 
action,  or  unpleasant  subjective  symptoms.  Massage  and  passive 
motion  have  also  some  value  as  added  therapeutic  aids  in  long-con- 
tinued cardiac  decompensation  in  bedridden  patients.  The  chief 
contraindication  in  such  individuals  is  extreme  continued  dyspnoea. 
In  such  cases,  massage  should  be  limited  to  the  extremities  and  to  the 
muscles  of  the  back ;  the  abdomen  and  anterior  part  of  the  chest  should 
not  be  included.  When  edema  and  venous  stasis  are  present,  it  may 
be  of  advantage  to  stroke  the  limbs  in  the  direction  of  the  venous  and 
lymphatic  current,  i.e.  from  the  periphery  to  the  trunk.  This  some- 
times decreases  the  local  engorgement. 

The  kind  of  massage  to  be  employed  in  cases  of  restored  compensa- 
tion must  be  individualized.  Usually  light  superficial  massage  alone 
is  tolerated.  Deep  vigorous  massage  and  kneading  of  the  muscles 
commonly  produces  discomfort  and  pain,  and,  by  exciting  the  patient, 
may  cause  rapid  heart  action  and  dyspnoea.  The  amount  of  passive 
motion  must  be  similarly  studied  in  every  individual  case.  Flexion 
and  extension  of  the  smaller  joints  —  the  fingers,  wrists,  ankles,  and 
toes  —  should  at  first  be  practiced  gently  once  daily ;  later,  the  larger 
joints  (knees,  elbows,  hips,  and  shoulders)  should  be  flexed  and  extended. 
If  these  procedures  are  not  followed  by  pain,  cyanosis,  tachycardia, 
exhaustion,  or  dyspnoea,  more  vigorous  and  oft-repeated  passive  motion 


224  CLINICAL   CARDIOLOGY 

can  be  employed.  Massage  and  passive  motion  do  not  necessarily 
require  the  services  of  a  trained  attendant ;  in  any  case,  however,  they 
should  at  the  outset  be  carried  out  under  the  direct  supervision  of  the 
medical  attendant,  so  that  he  can  carefully  observe  any  possible  ill 
effects  following  their  use. 

Calisthenics  —  Medical  Gymnastics  —  Resistance  Exercises.  — 
These  are  occasionally  indicated  while  the  patient  is  still  in  bed.  They  re- 
quire the  more  active  cooperation  of  the  patient  and  make  more  demands 
upon  his  circulatory  reserve.  Rapid  breathing,  dyspnoea,  increased 
and  prolonged  pulse  rapidity,  or  subjective  feelings  of  faintness  and 
exhaustion  are  the  best  clinical  guides  that  gymnastics  or  exercise  have 
exceeded  safe  limits  and  have  caused  marked  diminution  of  the  cardiac 
reserve  power.  It  should  be  emphasized  that  these  treatments  are 
only  added  therapeutic  aids,  and  cannot  replace  circulatory  drugs  when 
indicated.  The  use  of  dumb-bells  and  of  carefully  graduated  exercises 
as  measured  by  the  ergostat  are  also  of  value.  According  to  some  ob- 
servers, delayed  return  to  the  normal  blood  pressure  following  dumb- 
bell exercise  constitutes  a  good  reaction,  and  is  to  be  regarded  as 
evidence  of  good  cardiac  reserve  power. 

Walking  is  the  best,  simplest,  and  most  accessible  of  all  the  forms  of 
more  active  exercise.  Some  years  ago,  a  system  of  carefully  planned 
and  graduated  hill  climbing  with  interspersed  resting  benches  was 
popular  on  the  continent  (Oertel  treatment),  but  arbitrary  insistence 
upon  fixed  distances  to  be  covered  or  hills  to  be  climbed  leaves  out  of 
consideration  the  only  safe  and  cardinal  guide  of  circulatory  endurance ; 
namely,  the  patient's  cardiac  reserve  power  as  measured  by  his  sub- 
jective sensations,  a  factor  which  varies  daily  or  even  hourly.  On  the 
other  hand,  walking  at  a  moderate  pace  on  the  level  or  up  a  slight  incline 
for  a  distance  or  length  of  time  well  within  the  patient's  circulatory 
power  is  a  much  safer  and  more  elastic  rule,  and  approaches  more 
nearly  the  normal  demands  and  mode  of  life  that  the  individual  will 
later  follow. 

Hydrotherapy.  —  The  usual  hydrotherapeutic  procedures  consist 
in  tepid  baths,  sponging  with  tepid  water  followed  by  a  quick  cool  or 
cold  sponge  over  the  entire  or  upper  parts  of  the  body,  tepid  or  cool 
shower  baths,  needle  baths,  or  sprays  of  water  of  varying  temperatures 
applied  to  various  portions  of  the  body.  Except  for  very  warm  baths, 
after  the  patient  is  properly  inured  to  them,  the  above  measures  are 
applicable  to  any  type  of  cardiac  disease  in  which  compensation  has 
been  well  established.  These  measures  have  their  especial  application, 
however,  in  a  large  group  of  patients  who,  in  addition  to  their  organic 
disease,  suffer  from  marked  neuropathic  tendencies.  Such  individuals 
are  apt  to  have  vasomotor  instability,  such  as  hot  or  cold  extremities, 
frequent  flushes,  etc.  They  may  suffer  from  dyspnoea  of  purely  sub- 
jective origin  not  correlated  with  exercise  or  with  any  discernible  cardiac 
change.     They  complain  of  indefinite  pains  in  the  chest,  neck,  or  arms. 


THERAPY  IN   CIRCULATORY  DISEASE  225 

They  frequently  suffer  from  headache  and  anorexia.  In  other  words, 
this  type  of  patient,  well  compensated,  suffers  from  that  train  of  cardiac 
symptoms  found  in  the  so-called  cardiopathic  individuals,  in  whom  there 
is  no  organic  disease.  Doubtless  the  knowledge  of  the  presence  of  organic 
trouble  plays  a  role  in  unduly  directing  the  patient's  attention  to  other- 
wise trivial  symptoms.  To  some  extent,  also,  I  have  found  that  this 
neuropathic  tendency  has  been  caused  by  consultation  with  physicians 
who  have  exaggerated  the  importance  of  the  physical  ailment  and  have 
not  sufficiently  relieved  the  mental  disquietude  and  fear  of  sudden  death 
which  exists  in  many  patients  with  cardiac  disease.  Naturally,  where 
pathological  changes  are  present,  it  will  require  careful  discrimination 
between  the  so-called  neurotic  symptoms  and  those  emanating  from  the 
organic  lesion.  In  those  in  whom  the  diagnosis  of  an  added  neurotic 
ailment  has  been  established,  the  hydrotherapeutic  measures  already 
outlined  exercise  a  very  favorable  influence.  Regarding  the  special 
procedure  to  be  employed  in  individual  instances,  it  is  necessary  to 
remember  that  in  no  case  should  early  treatments  be  so  brusque  or 
rigorous  as  to  frighten  or  in  any  way  upset  the  patient.  Tepid  baths 
or  sponges  should  be  employed  at  first ;  'later,  more  vigorous  measures  — 
cool  sprays  and  showers  —  may  be  used.  In  this  manner,  the  neurotic 
symptoms,  which  are  very  real  and  often  disheartening  to  the  patient, 
may  gradually  disappear. 

Carbon  Dioxide  and  Oxygen  Baths.  —  In  a  different  therapeutic 
category  belong  those  baths  in  which  the  water  is  naturally  or  artificially 
charged  with  carbon  dioxide  or  oxygen.  The  gas  bubbles  surround  the 
body  of  the  patient,  produce  a  sensation  of  warmth,  and  cause  dilatation 
of  the  superficial  vessels.  The  claim  is  made  that  by  the  use  of  these 
gas-impregnated  baths,  congestion  is  relieved,  the  pulse  rate  slowed, 
dyspnoea  decreased,  and  the  overburdened  heart  correspondingly 
benefited.  There  are  conflicting  reports  regarding  the  effect  of  these 
baths  upon  blood  pressure ;  it  is  raised  according  to  some,  lowered 
according  to  others.  In  those  I  have  observed,  there  was  no  constant 
rise  or  fall  of  the  systolic  blood  pressure  following  the  baths.  There 
seems  little  room  for  doubt,  that,  when  taken  at  Spas  and  health  resorts, 
gas-impregnated  baths  are  of  benefit;  this  is  not,  however,  because  of 
their  direct  effect  upon  the  circulation,  but  because  of  the  difference 
in  environment  and  enforced  rest  from  business  and  worry,  and  because 
of  the  more  moderate  diet  and  more  regular  and  physiological  mode  of 
living.  The  baths  act  upon  the  circulation  in  the  same  manner  as  a 
mild  stimulating  exercise,  and,  in  my  opinion,  upon  this  alone  rests 
their  efficacy  upon  the  circulation.  Their  use  should  therefore  be 
limited  to  well-compensated  patients  or  to  those  with  mild  disturbances 
of  compensation.  Even  here,  the  baths  should  not  be  prescribed  uni- 
versally, but  only  to  those  in  whom  observation  has  shown  a  good  reaction 
during  and  following  the  bath.  Cold  extremities,  a  sense  of  exhaustion, 
rapid  breathing,  accelerated  pulse  rate,  dyspnoea,  constitute  distinct 


226  CLINICAL   CARDIOLOGY 

contraindications.     I  regard  the  possible  effect  upon  the  blood  pressure 
as  of  less  importance. 

The  usual  routine  of  a  series  of  carbonated  baths  given  at  Nauheim 
consists  of  a  first  immersion  lasting  from  five  to  seven  minutes  in  a  bath 
of  the  temperature  of  95°  F.  The  temperature  of  the  succeeding  baths 
is  gradually  reduced  to  about  86°  F.  and  the  immersion  time  slowly 
increased  to  20  minutes.  The  bath  is  omitted  every  third  or  fourth 
day.  A  full  course  consists  of  two  series  of  20  baths  each,  with 
an  interval  of  three  or  four  weeks.  Oxygen  and  '  Nauheim '  car- 
bonated brine  baths  can  be  prepared  at  home  by  dissolving  salts 
producing  oxygen  and  carbon  dioxide  gas  respectively,  in  a  proper 
quantity  of  water.  Naturally  the  greatest  disadvantage  of  such  home 
baths  is  that  there  is  no  change  of  environment,  with  all  its  attendant 
and  important  beneficial  features.  However,  in  the  group  of  cardiac 
patients  already  described,  who  suffer  largely  from  neurotic  in  addition 
to  organic  complaints,  gas-impregnated  baths,  even  when  taken  at 
home,  may  be  followed  by  excellent  results. 

Types  of  Patients  Suitable  for  Spa  Treatment.  —  The  question 
frequently  and  insistently  arises  in  private  practice  as  to  the  class  of 
cardiac  patients  who  should  be  sent  to  the  continent  for  'Nauheim' 
treatment.  Nauheim  is  mentioned  because  it  is  the  most  popular  and 
best  known  among  the  patients  themselves.  Until  some  American 
health  resort  becomes  as  popular  and  can  offer  the  same  or  similar 
well-balanced  facilities  for  restful  environment  and  medical  supervision, 
the  question  must  be  fairly  met  and  intelligently  considered.  The 
answer  must  depend,  not  upon  the  type  of  valvular  lesion  or  cardio- 
vascular disease,  but  chiefly  upon  the  state  of  cardiac  compensation. 
Patients  severely  decompensated,  for  example  those  suffering  from  marked 
edema,  cyanosis,  and  dyspncea,  should  be  advised  against  taking  a 
trip  abroad  for  Spa  treatment.  They  are  more  benefited  by  proper 
treatment  at  home.  There  are  some  patients,  however,  otherwise 
intelligent,  who  will  go  to  almost  untold  risks  and  expense  to  achieve 
what  they  conceive  to  be  a  life-saving  cure,  and  this  directly  against 
medical  advice.  I  have  observed  several  such  patients  who  returned 
home  worse  than  when  they  left;  very  few  were  improved.  One  of 
those  not  benefited  was  a  physician  with  riiarked  cardiosclerosis,  edema, 
and  cyanosis,  who  left  for  Europe  against  advice ;  he  returned  home  a 
few  months  later  in  extremis.  The  patients  I  have  found  most  improved 
were  those  who,  besides  mild  decompensation,  were  nervous,  high-strung, 
or  worried,  and  who  at  the  foreign  Spas  were  able  not  only  to  have 
enforced  rest  and  quiet,  but  also  to  quickly  divorce  their  minds  and 
thoughts  from  domestic  and  business  cares.  It  is  to  individuals  of  this 
type  that  Spa  treatment  should  be  recommended  with  the  great  prob- 
ability that  it  will  be  followed  by  good  results. 

Tonsillectomy  is  discussed  in  this  connection  because  it  has  assumed 
much  importance  since  the  demonstration  that  the  tonsils  are  often 


THERAPY  IN   CIRCULATORY  DISEASE  227 

the  portals  of  entry  for  endocardial  infections.  Tonsils  which  are 
palpably  diseased  or  which  become  frequently  infected,  should  be  prop- 
erly and  thoroughly  removed  if  the  general  condition  of  the  patient 
warrants  it.  This  statement  also  applies  to  adenoids.  However,  I 
hold  conservative  views  regarding  the  removal  of  apparently  healthy 
tonsils  with  the  idea  of  preventing  the  further  spread  of  endocarditis: 
I  believe  that  when  valvular  disease  is  already  present,  the  removal 
of  small  and  healthy  looking  tonsils  does  not  tend  to  prevent  reinfection. 
This  view  is  not  invalidated  by  the  fact  that  tonsils  which  look  normal 
in  the  throat  show,  upon  removal,  various  pathological  changes,  both 
macro-  and  microscopically.  Because  of  their  function  as  filtering 
agents  and  constant  contact  with,  and  exposure  to,  bacteria,  the  tonsils 
can  scarcely  ever  represent  normal  lymphoid  structures.  It  is  still  a 
moot  question  whether  recrudescences  of  endocarditis  have  been  pre- 
vented by  the  routine  and  radical  practice  of  tonsillectomy  in  all  children 
with  valvular  lesions.  Thus,  in  one  excellent  report,  such  tonsillec- 
tomies did  not  affect  the  frequency  of  recurrences,  nor  the  course  of  the 
disease. 

Extraction  of  Teeth.  —  As  the  result  of  careful  and  long-continued 
observation,  I  believe  that  endocarditis  in  itself  does  not  warrant  more 
radical  or  careful  dentistry  than  is  usually  required  for  diseased  teeth 
and  purulent  foci  in  other  otherwise  normal  individuals.  Dentistry 
here  as  elsewhere  should  follow  sane  lines.  As  with  tonsillectomy,  I 
regard  routine  extraction  for  the  prevention  of  endocarditis  as  uncalled 
for  (Chapter  XI).  Extensive  extractions  upon  the  supposition  that 
exceedingly  small  pus  foci  frequently  produce  endocarditis  is  in  my 
opinion  unwarranted  by  general  clinical  experience  and  by  the  negative 
results  following  such  practice  in  patients  with  endocarditis. 


REFERENCES 
Chapter  XVI 

Barringer,  T.  B.,  Jr.,  and  Teschner,  J. :  The  Treatment  of  Cardiac  Insuffi- 
ciency, etc.,  with.  Dumbbells  and  Bars  ;  Archives  of  Internal  Medicine,  1915, 
XVI,  795. 

Cohn,  A.  E. :  Present  Status  of  the  Electrocardiographic  Method  in  Medicine  ; 
American  Journal  of  the  Medical  Sciences,  1916,  CLI,  529. 

Cohn,  A.  E.,  and  Fraser,  F.  R. :  Certain  Effects  of  Digitalis  on  the  Heart ; 
International  Medical  Congress,  1913,  Section  6,  Part  II,  258. 

Cohn,  A.  E.,  and  Lewis,  T. :  Auricular  Fibrillation  and  Complete  Heart  Block ; 
Heart,  1912-1913,  IX,  17. 

Cushny,  A.  R. :   Pharmacology  and  Therapeutics  of  the  Action  of  Drugs. 

Eggleston,  C. :  Digitalis  Dosage ;  Archives  of  Internal  Medicine,  1915,  XVI,  1. 

Eggleston,  C,  and  Hatcher,  R.  A. :  The  Emetic  Action  of  the  Digitalis  Bodies ; 
Journal  of  American  Medical  Association,  1913,  LX,  499. 

Neuhof ,  S. :  Intravenous  Injections  of  Theobromine  Sodium  Salicylate ;  New 
York  Medical  Journal,  October  25,  1913. 

Price,  F.  W. :  Some  Investigations  of  the  Action  of  Digitalis,  on  the  Blood 
Pressure  in  Man  ;  British  Medical  Journal,  1912,  II,  689. 


228  CLINICAL  CARDIOLOGY 

Rudolf,  R.  D.,  and  Cole,  C.  E.  C. :   The  Effects  of  Medicinal  Doses  of  Aconite 

upon  the  Pulse  Rate ;  American  Journal  of  Medical  Sciences,  1912,  CXLIV, 

788. 
von  Schroeder,  W. :  Ueber  die  diuretische  Wirkung  des  Kaffeins,  etc. ;  Archiv 

f .  Exptl.  Path,  und  Pharmakologie,  XXIV,  85. 
Schlayer,  C. :    Verhandlungen  des  XX Vllten  Kongresses  f .  innere  Medizin ; 

1910,  744. 
Taussig,  A.  E. :    Complete  and  Permanent  Heart  Block  following  the  Use  of 

Digitalis  in  Auricular  Fibrillation ;    Archives  of  Internal  Medicine,  1912, 

X,  335. 
Turnbull,  H.  H. :  Cardiac  Irregularities  produced  by  Squills;  Heart,  1910-1911, 

II,  15. 
Windle,  J.  D. :    Heart  Block  from  Drugs  of  the  Digitalis  Group;  Heart,  1911- 

1912,  III,  1. 


CHAPTER  XVII 

DIET,  AND  RENAL  AND  BLOOD  TESTS  IN  CARDIAC  DISEASE 

From  the  dietetic  standpoint,  and  because  of  the  frequent  correla- 
tion of  cardiac  with  renal  disease,  it  is  necessary  to1  make  a  clinical 
distinction  between  purely  cardiac  cases  with  no  or  very  slight  secondary 
renal  involvement,  and  those  in  whom  renal  involvement  is  the  primary 
or  predominant  feature.  It  is  also  necessary,  in  both  types,  to  remember 
that  we  are  dealing  with  chronic  conditions,  and  that  the  dietetic 
regime  will  have  to  be  carried  out  for  months  and  years.  Hence  the 
diet  should  not  be  unnecessarily  harsh  or  restricted,  and  consideration 
should  be  given,  as  far  as  possible,  to  individual  idiosyncrasies  and 
tastes. 

In  patients  with  compensated  valvular  disease  with  or  without 
hypertrophy,  without  renal  involvement  or  hypertension,  it  is  not  nec- 
essary to  make  any  radical  change  from  the  usual  dietary  of  balanced 
rations  of  an  individual  in  health.  There  is  no  necessity  for  strict  ob- 
servance of  any  special  diet,  nor  for  the  limitation  of  fluids.  On  the 
other  hand,  there  should  be  sensible  restriction  about  excesses  of  any 
kind  of  food  or  drink. 

The  Use  of  Beverages.  —  To  patients  who  have  been  accustomed 
to  small  amounts  of  alcohol  in  the  form  of  beer  or  light  wines,  I  have 
been  in  the  habit  of  allowing  a  slight  amount  of  these  beverages,  pro- 
vided observation  shows  no  deleterious  effects  upon  the  circulation  as 
noted  by  the  pulse  rate  and  blood  pressure.  I  have  usually  limited 
the  amount  to  one  glass  of  beer  or  to  a  small  glass  of  light  wine  taken 
at  the  principal  meal.  I  have  observed  such  patients  for  years,  and 
I  have  found  no  ill  effects  upon  the  cardiac  condition  ascribable  to  this 
practice.  Similarly,  if  patients  have  been  in  the  habit  of  taking 
tea  or  coffee  without  any  ill  effects,  a  cup  of  weak  tea  or  coffee  may 
be  allowed  daily.  In  obese  individuals,  the  carbohydrate  and  fat 
intake  should  be  somewhat  restricted  in  order  to  produce  some  loss  in 
weight ;  but  this  should  be  a  gradual  process  and  so  fitted  to  individual 
needs  that  the  diet  does  not  become  irksome,  and  hence  apt  to  be  given 
up.  As  substitutes  for  carbohydrates  and  fats,  cabbage,  spinach, 
lettuce,  beans,  carrots,  and  mushrooms  may  be  suggested. 

229 


230  CLINICAL  CARDIOLOGY 

Those  with  myocardial  insufficiency  and  dyspnoea  without  edema 
are  usually  too  ill  to  relish  a  normal  amount  of  solid  food,  so  that 
the  patient's  own  limitations  and  dietetic  inclinations  are  usually 
sufficiently  safe  guides.  But  in  view  of  the  possibility  of  visceral 
stasis  and  of  edema,  the  fluid  intake  should  be  somewhat  restricted; 
about  500  c.c.  in  addition  to  solid  and  semisolid  nourishment  is  a  safe 
limit.  In  cases  of  myocardial  insufficiency  with  edema,  pleuritic  trans- 
udates, or  marked  visceral  congestion,  a  strict  Karrell  diet  for  several 
successive  days  or  in  courses  of  several  days  each,  as  already  outlined  in 
the  discussion  of  theobromine  (Chapter  XVI),  is  an  excellent  aid  to 
drug  therapeusis.  The  Karrell  diet  reduces  the  salt  intake  to  a  mini- 
mum. Even  after  disappearance  of  edema,  and  when  comparison  of 
the  salt  intake  with  its  output  in  the  urine  proves  a  normal  relation- 
ship and  no  chloride  retention,  only  a  moderate  amount  of  salt  should 
be  allowed,  in  order  to  overcome  any  tendency  to  edema  by  salt  reten- 
tion. 

The  importance  of  diet  in  those  cardiorenal  cases  in  which  the 
kidneys  especially  require  attention  requires  a  brief  account  of  some 
of  the  modern  methods  of  kidney  study  and  diagnosis,  and  their  corre- 
lation with  diet  and  therapy.  Besides  the  routine  examination  of  the 
urine  for  normal  and  abnormal  chemical  and  microscopical  constituents, 
other  methods  have  come  into  use  to  estimate  renal  function  and  effi- 
ciency by  the  power  of  elimination  of  certain  substances  or  foods  taken 
internally  or  given  subcutaneously.  The  status  and  value  of  some  of 
these  tests  and  their  correlation  with  clinical  data  have  not  yet  been 
definitely  fixed.  Two  of  these  tests  consist  in  the  study  of  iodide  of 
potash  excretion,  and  of  the  elimination  of  lactose  injected  intrave- 
nously. Both  of  these  have  been  practically  discarded.  The  first  test 
requires  a  long  time  for  its  completion  and  gives  inaccurate  results; 
the  lactose  test  is  too  cumbersome  and  is  likewise  inaccurate.  Probably 
the  most  important  method  at  the  present  time  consists  in  the  estimation 
of  the  excretion  percentage  in  the  urine  of  a  dye  which  is  injected  sub- 
cutaneously. Phenolsulphophthalein  is  usually  chosen  for  this  study. 
Briefly,  the  method  employed  is  as  follows  :  — 

Twenty  minutes  to  one-half  hour  before  the  injection,  the  patient 
is  given  200  to  400  c.c.  of  water.  The  patient  is  then  catheterized,  the 
time  noted,  and  the  catheter  kept  in  place.  One  c.c.  of  a  carefully 
prepared  sterile  solution,  containing  6  m.g.  of  the  dye,  is  injected  intra- 
muscularly in  the  lumbar  region.  The  urine  is  allowed  to  drain  into  a 
test  tube  which  contains  a  drop  of  a  25  per  cent  sodium  hydroxide 
solution,  and  the  time  of  the  appearance  of  the  first  pinkish  tinge  is 
noted.  The  catheter  is  then  withdrawn  and  the  patient  is  asked  to  void 
into  two  different  receptacles  at  the  end  of  one  and  two  hours  respec- 
tively. Sufficient  25  per  cent  sodium  hydroxide  solution  is  added 
to  make  the  urine  decidedly  alkaline.  This  causes  a  yellowish  or  orange 
color  in  acid  urines  which  suddenly  changes  to  a  brilliant  purplish 


DIET,   AND  RENAL  AND   BLOOD   TESTS  231 

red  when  the  urine  becomes  alkaline.  Sufficient  water  is  now 
added  to  each  specimen  to  make  1000  c.c.  The  solution  is  mixed ; 
a  small  portion  is  then  filtered  and  compared  with  the  standard  color. 
In  those  patients  seen  in  office  consultation,  where  the  phthalein  test 
seems  of  value,  I  have  employed  the  following  routine :  The  patient  is 
asked  to  void ;  he  is  then  given  a  glass  of  water  and  the  dye  is  injected. 
He  is  sent  home  and  is  asked  to  void  his  urine  two  hours  after  the  in- 
jection; this  specimen  is  then  examined  for  the  percentage  of  dye 
excretion.  I  have  found  this  method  sufficiently  exact  for  ordinary 
purposes ;  it  obviates  the  necessity  for  catheterization,  and  requires 
very  little  time. 

As  colorimeters  the  Dunning,  Hellige,  or  Duboscq  instruments  may 
be  used ;  or  one  can  manufacture  as  I  have  done  a  practical  and  suffi- 
ciently accurate  colorimeter  by  using  a  series  of  bottles  or  tubes  which 
contain  the  solution  of  phenolsulphophthalein  in  multiples  of  5  per  cent ; 
the  tubes  are  sealed  and  their  respective  percentage  labeled ;  they 
may  then  be  used  as  color  standards.  If  the  dye  first  appears  in  the 
urine  within  15  minutes  of  the  time  of  its  injection,  and  40  to  50  per 
cent  is  excreted  within  two  hours,  the  test  is  regarded  as  normal.  For 
clinical  purposes,  the  two-hour  excretion  test  alone  is  sufficient;  this 
saves  catheterization  of  the  patient.  In  both  renal  congestion  secondary 
to  circulatory  disturbances  and  in  contracted  kidney,  the  percentage 
and  output  in  two  hours  is  usually  decreased.  It  requires  the  clinical 
examination  to  determine  which  of  the  two  factors  —  renal  congestion 
or  primary  nephritis  —  is  the  cause  of  the  decreased  phthalein  output. 

For  the  purpose  of  testing  quantitatively  for  urea,  salt,  and  water 
output  in  the  urine,  a  balanced  diet  containing  a  measured  amount  of 
solids  (starches,  sugar,  fats,  proteids,  and  salts)  and  of  fluids  (milk, 
water,  tea)  is  given.  Schlayer's  diet  or  some  modification  may  be 
employed.  An  excellent  and  well-balanced  ration  is  that  prescribed  by 
Mosenthal  for  testing  the  renal  function.     This  is  as  follows :  — 


Nephritic   Test   Diet 

All  food  is  to  be  salt  free. 

Salt  for  each  meal  is  furnished  in  weighed  amounts.1 

All  food  or  fluid  not  taken  must  be  weighed  or  measured  after  meals, 
and  charted. 

Allow  no  food  or  fluid  of  any  kind  except  at  meal  times. 

Note  any  mishaps  or  irregularities  that  occur  in  giving  the  diet  or 
collecting  the  specimens. 

1  One  capsule  of  salt,  containing  2.3  gm.  of  sodium  chloride,  is  furnished  for 
each  meal.  The  salt  which  is  not  consumed  is  returned  to  the  laboratory, 
where  it  is  weighed,  and  the  actual  amount  of  salt  taken  is  calculated. 


232  CLINICAL  CARDIOLOGY 

Breakfast,  8  a.m.  Dinner,  12  Noon. 

Boiled  oatmeal,  100  gm.  Meat  Soup,  180  c.e. 

Sugar,  1-2  teaspoonful  Beefsteak,  100  gm. 

Milk,  30  c.e.  Potato  (baked,  mashed,  or  boiled),  130  gm. 

Two  slices  bread  (30  gm.  each.)  Green  vegetables,  as  desired 

Butter,  20  gm.  Two  slices  bread  (30  gm.  each) 

Coffee,  160  c.e.  1  Butter,  20  gm. 

Sugar,  1  teaspoonful  >  200  c.e.  Tea,  180  c.e.  "| 

Milk,  40  c.e.  J  Sugar,  1  teaspoonful  }  200  c.e. 

Milk,  200  c.e.  Milk,  20  c.e.  J 

Water,  200  c.e.  Water,  250  e.c. 

Pudding  (tapioca  or  rice,)  110  gm. 

Supper,  5  p.m. 

Two  eggs,  cooked  in  any  style 

Two  slices  bread  (30  gm.  each) 

Butter,  20  gm. 

Tea,  180  c.e.  ] 

Sugar,  1  teaspoonful  >  200  c.e. 

Milk,  20  c.e.  J 

Fruit  (stewed  or  fresh),  1  portion 

Water,  300  c.e. 

8  a.m.  —  No  food  or  fluid  is  to  be  given  during  the  night  or  until 
8  o'clock  the  next  morning  (after  voiding),  when  the  regular  diet  is 
resumed. 

Patient  is  to  empty  bladder  at  8  a.m.  and  at  the  end  of  each  period, 
as  indicated  below.  The  specimens  are  to  be  collected  for  the  following 
periods  in  properly  labeled  bottles  : 

8  a.m-10  a.m.  ;  10  a.m-12  n.  ;  12  N.-2  p.m.  ;  2  P.M.-4  p.m.  ;  4  p.m.- 
6  p.m.  ;  6  P.M.-8  p.m.  ;  8  p.m.  -8  a.m. 

Outside  of  hospitals,  as  in  sanatoria  or  at  home,  a  similar  dietetic 
regime  can  be  carried  out  if,  instead  of  quantities  measured  in  grams 
and  cubic  centimeters,  their  known  equivalents  in  cupfuls,  glasses,  and 
teaspoonfuls  be  substituted.  This  is  a  modification  that  I  have  carried 
out  where  careful  weighing  of  the  various  food  constituents  could  not 
be  done,  and  I  have  found  the  results  sufficiently  accurate  for  clinical 
purposes. 

The  amounts,  specific  gravity,  and  sodium  chloride  content,  and  the 
urea  determination  by  the  hypobromite  method  or  preferably  the 
nitrogen  content  by  the  Kjeldahl  method  are  separately  determined 
for  each  two-hourly  specimen,  and  also  for  the  night  specimen.  In 
other  words,  there  are  six  determinations  for  the  day,  and  one  for  the 
night  specimen.  In  this  manner,  besides  other  data,  a  comparison  of 
the  amounts  and  specific  gravity  of  the  day  and  night  urines  is  made. 
If  the  specific  gravity  is  low  and  shows  only  slight  variations  in  the 
different  specimens,  and  the  night  urine  is  larger  in  amount  than  that 
voided  during  the  day,  this  speaks  for  the  presence  of  a  chronic  intersti- 
tial nephritis. 


DIET,   AND   RENAL  AND   BLOOD  TESTS  233 

Because  of  evaporation  by  the  lung  and  elimination  of  water  by  the 
skin  and  intestines,  the  amount  of  urine  is  normally  less  than  the  fluid 
intake.  Approximately  all  sodium  chloride,  and  about  90  per  cent  of 
the  nitrogen  ingested,  is  excreted  by  the  urine.  Thus,  the  chemical 
urine  tests  above  indicated  give  valuable  information  regarding  the 
retention  of  salt  and  nitrogenous  products  in  the  body. 

In  order  to  determine  which  of  these  chemical  tests  is  of  most  clinical 
value,  I  have  added  in  a  small  series  of  cases  a  study  of  the  non-protein 
nitrogen  in  the  blood,  the  estimation  of  carbon  dioxide  tension  of  the 
expired  air  by  means  of  the  Fredericia  apparatus,  and  the  phthalein 
output ;  I  have  also  observed  the  alkali  tolerance  of  the  urine  by  giving 
the  patient  measured  amounts  of  bicarbonate  of  soda  until  the  urine 
became  alkaline.  I  have  not  yet  arrived  at  any  definite  conclusions. 
However,  I  believe  that  a  very  careful  study  of  the  clinical  phenomena, 
of  the  amount  and  concentration  of  the  night  urine,  and  of  the  ordinary 
examination  of  several  specimens  of  urine  taken  within  24  hours,  will 
allow  us  to  judge  with  sufficient  clinical  accuracy  the  amount  and  type 
of  the  retained  excrementitious  products  and  even  of  the  degree  of 
renal  insufficiency  in  the  majority  of  cases.  In  other  words,  clinicians 
may  soon  hope  to  reap  the  advantages  of  the  careful  scientific  work 
of  the  laboratory  by  comparison  of  its  results  with  ordinary  bedside 
methods. 

Chemical  examination  of  the  blood  has  assumed  great  importance, 
especially  since  simpler  and  accurate  methods  have  replaced  the  former 
cumbersome  and  less  accurate  determinations.  The  important  constitu- 
ents sought  for  are  non-protein  nitrogen,  creatinine,  and  uric  acid.  The 
knowledge  thus  gained  is  not  yet  fixed  or  positive,  but  there  seems 
to  be  a  correlation  between  an  abnormal  amount  of  non-protein  nitrogen 
retained  in  the  blood,  a  decreased  phthalein  output,  and  clinical  evidence 
of  a  severe  nephritis  of  predominant  vascular  type.  Not  only  has  our 
diagnostic  and  prognostic  knowledge  been  enhanced  by  these  blood 
examinations,  but  the  dietary  of  nephritis  has  assumed  a  more  rational 
and  scientific  aspect.  The  subject  of  salt  restriction  has  already  been 
mentioned.  In  nephritics  with  abnormally  increased  amounts  of  non- 
protein nitrogen  in  the  blood,  a  low  protein  and  high  carbohydrate 
diet  is  indicated.  The  amount  of  fluid  should  be  restricted  if  urine 
measurements  show  decreased  elimination  of  water.  If  the  amount 
of  urinary  excretion  is  normal,  it  is  advisable  to  occasionally  allow 
large  quantities  of  fluids  —  as  much  as  several  liters  within  24  hours  — 
in  the  attempt  to  flush  the  system  and  thus  get  rid  of  toxic  products. 

In  nephritis  with  excessive  and  abnormal  amounts  of  non-protein 
nitrogen  in  the  blood,  attempts  have  been  made  to  therapeutically 
attack  the  disease  upon  a  chemical  basis.  Sugar  solutions  have  been 
administered  intravenously  or  by  the  Murphy  drip.  In  cases  of  lessened 
blood  alkalinity  (so-called  acidosis),  I  have  in  several  cases  given  in- 
travenous injections  of  500  c.c.  of  a  5  per  cent  solution  of  bicarbonate  of 


234  CLINICAL   CARDIOLOGY 

soda.  One  instance  was  that  of  a  patient  of  64  with  cardio-nephritis, 
regular  pulse,  hypertension,  general  anasarca,  and  nocturnal  dyspnoea, 
who  had  been  ill  over  one  year.  Therapy  consisting  in  digitalis,  theo- 
bromine, appropriate  diet,  and  occasional  Karrell  days  over  a  period 
of  several  weeks,  had  only  a  very  slight  influence  upon  the  symptoms  and 
course  of  the  disease.  500  c.c.  of  blood  were  withdrawn  by  venesection 
and  the  same  amount  of  a  5  per  cent  bicarbonate  solution  injected. 
Within  24  hours  improvement  began  and  continued  uninterruptedly. 
At  the  end  of  two  weeks,  edema  and  dyspnoea  had  entirely  disappeared. 
In  another  case,  a  man  with  cardiovascular  disease,  a  systolic  blood 
pressure  of  250,  aortitis,  very  marked  left  ventricular  hypertrophy,  and 
attacks  of  nocturnal  dyspnoea  relieved  only  by  morphine,  a  similar 
procedure  was  employed.  The  injection  was  followed  by  improvement 
for  several  days.  In  less  urgent  cases  I  have  tried  venesection  combined 
with  a  10  per  cent  bicarbonate  solution  per  rectum  given  by  the  Murphy 
drip.  Possibly  a  simple  bedside  method  like  the  use  of  the  Fridericia 
apparatus  for  the  determination  of  C02  content  in  the  alveolar  air 
may  give  sufficiently  accurate  estimations  parallel  to  the  chemical 
examination  of  the  blood  for  acidosis,  and  thus  be  of  advantage  in 
determining  the  cases  suitable  for  alkaline  therapy. 

REFERENCES 
Chapter  XVII 

Folin,  0.,  and  Denis,  W. :  On  the  Creatinine  Content  of  the  Blood ;  Journal  of 
Biological  Chemistry,  1914,  XVII,  487. 

Folin,  O.,  Denis,  W.,  and  Seymour,  M. :  The  Non-protein  Nitrogenous  Constit- 
uents of  the  Blood  in  Chronic  Vascular  Nephritis,  etc. ;  Archives  of  In- 
ternal Medicine,  1914,  XIII,  224. 

Mosenthal,  H.  O. :  Renal  Function  as  Measured  by  the  Elimination  of  Fluids, 
etc. ;  Archives  of  Internal  Medicine,  1915,  XVI,  733. 

Rowntree,  L.  G.,  and  Gerarghty,  J.  T. :  An  Experimental  and  Clinical  Study  of 
Phenolphthalein  in  Relation  to  the  Renal  Function ;  Archives  of  Internal 
Medicine,  1912,  IX,  284. 

Schlayer,  C. :  Verhandlungen  des  XXVIIten  Kongresses  f .  innere  Medizin, 
1910,  744. 


CHAPTER  XVIII 

MANAGEMENT    OF   CARDIAC   DISEASE  —  MARRIAGE   IN 
WOMEN   WITH   VALVULAR   DISEASE 

Aside  from  therapy  and  diet,  other  questions  regarding  the  manage- 
ment of  compensated  and  decompensated  cases  of  cardio-vascular 
disease  arise.  Some  of  the  commoner  of  these  are  :  Shall  a  patient  re- 
turn to  work  ?  What  type  of  work  shall  he  follow  ?  Shall  medication 
be  continued  and,  if  so,  how  long  ?  How  shall  reinfection  be  prevented  ? 
Shall  women  with  heart  disease  be  allowed  to  marry  ? 

With  respect  to  these  questions,  no  matter  what  the  type  of  lesion,  there 
are  two  preliminary  fundamental  considerations  to  be  determined,  namely : 
the  degree  of  compensation  and  the  state  of  quiescence  of  the  disease. 
With  quiescent  compensated  lesions,  valvular  or  myocardial  in  nature, 
the  main  restriction  regarding  exercise  should  be  the  kind,  rather  than  the 
amount,  provided  always  it  be  well  within  the  patient's  cardiac  reserve 
power.  This  statement  requires  some  modification,  for  the  type  of 
cardiac  disease  plays  a  role  which  requires  some  individual  discrimina- 
tion. For  example,  patients  with  tremendous  hypertrophic  left  ven- 
tricles from  aortic  valvular  lesions  are  scarcely  able  to  maintain  long- 
continued  effort  without  soon  encroaching  upon  their  cardiac  reserve. 
In  general,  however,  it  may  be  stated  that  even  quiescent  compensated 
cases  should  avoid  all  exercises  which  call  for  sudden  or  sharp  exertion, 
as  swimming,  running,  and  tennis  playing.  On  the  other  hand,  golf 
is  an  excellent  form  of  moderate  exercise.  It  entails  the  necessity  of 
being  away  from  business  and  out  in  the  open  for  a  number  of  hours, 
in  themselves  very  desirable.  In  exercise  as  well  as  in  work  it  should  be 
emphasized  that  patients  should  keep  well  within  their  individual 
limits  of  fatigue. 

The  question  of  occupation  and  vocation  for  patients  with  cardiac 
disease  has  recently  received  wide  consideration  from  the  lay  as  well 
as  from  the  medical  standpoints.  It  is  gradually  being  recognized 
that  many  individuals  with  cardiovascular  disease  are  not  thereby 
necessarily  precluded  from  attempting  to  earn  a  livelihood,  and  that,  if 
proper  work  be  chosen,  they  may  become  self-sustaining  members  of  the 
community.     Occupations  and  vocations  at  which  patients  sit  or  stand 

235 


236  CLINICAL  CARDIOLOGY 

are  preferable  to  those  which  require  walking  or  stair  climbing.  Posi- 
tions in  counting  houses,  clerical  work,  draftsmanship,  light  manu- 
facturing industries,  working  at  lathes  or  small  machinery,  watchmen, 
are  examples  of  the  work  which  these  patients  may  safely  follow ;  but 
just  because  of  these  sedentary  and  easy  occupations,  exercise  out  in 
the  open,  chiefly  walking,  should  be  advised.  It  is,  I  believe,  a  thera- 
peutic error  to  attempt  to  avoid  all  circulatory  strain  by  having  these 
patients  pass  an  almost  muscularly  inert  existence,  for  it  is  only  by 
mildly  stimulating  the  circulation  by  appropriate  gentle  exercise  that 
the  heart  and  circulatory  apparatus  are  kept  at  their  proper  individual 
level  of  efficiency .  In  this  respect  the  heart  does  not  differ  from  other 
weakened  muscles  whose  strength  is  enhanced  by  moderate,  well-planned, 
and  individualized  exercise.  Mild,  appropriate  dumb-bell  exercises  and 
other  calisthenics  should  be  advised  when  walking  is  not  feasible,  or 
as  additions  to  the  latter. 

In  this  connection,  a  brief  account  of  functional  efficiency  tests 
for  estimating  the  cardiac  reserve  power  is  appropriate.  Various  tests 
have  been  proposed  to  estimate  the  muscular  efficiency  and  working 
power  of  the  heart.  A  fluoroscopic  examination  is  one  means  which 
has  been  employed.  If  orthodiascopic  observation  reveals  an  increase 
in  the  size  of  the  cardiac  outline  after  exercise  (i.e.  if  the  heart  dilates 
instead  of  contracting),  it  is  regarded  as  a  sign  of  an  inefficient 
heart;  while  if  contraction  follows  exercise,  the  heart  is  regarded  as 
efficient.  Differences  in  systolic  blood  pressure  following  exercise,  and 
differences  in  pulse  pressure  in  the  standing  and  sitting  positions,  are 
also  employed  as  guides  of  cardiac  sufficiency.  An  attempt  has  like- 
wise been  made  to  estimate  the  muscular  efficiency  and  cardiac  load  by 
a  standard  quotient  obtained  by  dividing  the  pulse  pressure  by  the  sys- 
tolic pressure.  Another  formula  consists  in  estimating  the  heart  load 
as  the  resultant  of  the  division  of  the  pulse  pressure  by  the  diastolic ; 
this  should  normally  approximate  50  per  cent.  Still  another  test  for 
functional  efficiency  consists  in  the  observation  of  the  time  required 
for  the  blood  pressure  to  return  to  its  level  following  exercise.  It  has 
been  found  that,  in  normal  individuals,  the  systolic  blood  pressure  is 
raised  immediately  after  a  moderate  amount  of  work.  With  more 
severe  exercise,  the  maximum  systolic  pressure  is  not  reached  until  one 
or  more  minutes  after  exercise  had  ceased.  This  observation  has 
recently  been  applied  in  a  study  of  the  functional  capacity  of  diseased 
hearts ;  instead  of  an  ergometer  the  foot  pounds  of  exercise  or  work 
are  computed  by  the  use  of  dumb-bells  and  bars  of  various  weights ; 
these  are  lowered  and  raised  a  certain  number  of  times  to  known  heights. 

Objection  to  Functional  Efficiency  Tests.  —  It  appears  to  me  that 
there  are  several  objections  to  the  various  methods  of  using  blood 
pressure  readings  as  tests  for  cardiac  efficiency.  Blood  pressure  de- 
pends upon  important  factors  other  than  systolic  output  (Chapter 
XIX) ;    the  cardiac  rate  in  circulatory  failure  often  increases  dispro- 


MANAGEMENT   OF  CARDIAC   DISEASE  237 

portionately  to  pulse  pressure ;  increased  cardiac  work  does  not  neces- 
sarily imply  increased  systolic  output  or  increased  blood  pressure ; 
the  state  of  venous  distention  in  the  splanchnic  area  —  an  unknown 
factor  because  it  cannot  be  measured  —  may  considerably  influence 
and  vitiate  the  calculations.  Finally,  the  various  estimations  can  only 
give  temporary  information  regarding  the  circulation  at  the  time  the 
tests  are  made.  Far  simpler,  more  readily  applicable,  and  apparently 
as  accurate  as  the  above  tests,  is  the  usual  clinical  method  of  observ- 
ing the  patient  during  various  forms  of  exercise  —  standing,  walking, 
bending,  etc.,  —  and  of  estimating  the  cardiac  reserve  by  noting  the 
rapidity  of  pulse  and  respiration,  dyspnoea,  and  such  subjective  sensa- 
tions as  discomfort  and  exhaustion.  Information  derived  from  the 
patient's  subjective  sensations  is  of  special  importance,  and  cannot 
of  course  be  calculated  by  any  instrumental  method.  The  above 
routine  can  be  further  amplified  in  appropriate  cases  by  allowing  the 
patient  to  follow  his  ordinary  occupation,  if  not  too  laborious,  for  part 
of  or  the  entire  day,  and  then  noting  the  effect  upon  his  circulation  and 
cardiac  reserve.  Such  data,  in  addition  to  a  very  careful  clinical  ex- 
amination, are,  I  believe,  preferable  to  mathematical  "  efficiency  tests." 

When,  in  cardiac  disease,  compensation  has  long  since  been  estab- 
lished, drugs  of  the  digitalis  group  are  not  indicated.  It  is,  however, 
very  important  to  decide  whether  a  patient  who  suffers  only  occasionally 
from  cardiac  failure  should  continue  medication  after  compensation 
has  been  restored.  This  has  already  been  partially  discussed  (Chapter 
XVI).  When  signs  of  cardiac  failure  occur  readily  after  moderate 
exercise,  patients  should  be  continuously  under  the  effect  of  some  digi- 
talis preparation.  This  is  especially  true  of  the  cardiac  failure  accom- 
panying auricular  fibrillation;  prolonged  compensation  can  be  best 
maintained  by  administering  small  doses  of  digitalis  for  stated  periods ; 
for  example,  for  one  week  and  then  discontinuing  the  drug  for  a  similar 
or  longer  period.  Thereafter  smaller  doses  may  be  administered  in  a 
similar  manner.  In  patients  with  rhythmically  beating  hearts,  in  whom 
tachycardia  is  one  of  the  signs  of  decompensation,  the  bromides  may  be 
of  value  in  addition  to  digitalis. 


Marriage  of  Women  with  Valvular  Disease 

This  question  is  one  which  requires  careful  consideration.  The 
possible  dangers  arising  from  marriage  are  twofold :  the  strain  and 
excitement  incidental  to  coitus  and  that  from  pregnancy.  Regarding 
the  former,  I  have  seen  several  instances  of  hemoptyses  immediately 
following  coitus  in  patients  with  auricular  fibrillation,  and  in  one  with 
cardiosclerosis  and  hypertension.  I  have  also  observed  several  in  which 
intercourse  was  followed  by  violent  tachycardia.     With  one  exception, 


238  CLINICAL  CARDIOLOGY 

the  cardiac  condition  of  these  patients  would  have  been  considered  fairly 
satisfactory  under  usual  conditions. 

The  marriage  question  cannot  always  be  settled  upon  the  grounds 
of  health  alone,  although  that  is  naturally  the  phase  of  importance  to 
the  physician.  Some  writers  maintain  that  patients  with  heart  disease 
should  never  marry,  no  matter  what  the  type  of  lesion.  I  believe 
that  this  view  is  extreme.  One  frequently  encounters  mothers  of  large 
families  who  doubtless  have  had  valvular  disease  for  many  years,  and 
who  have  gone  safely  and  normally  through  pregnancy  and  parturition. 
Many  of  these  patients  were  never  aware  of  their  disease ;  in  some  the 
lesion  was  discovered  in  the  course  of  a  routine  examination. 

Marriage  should  naturally  not  be  considered  at  the  time  when  the 
patient  shows  the  slightest  degree  of  decompensation.  In  those  who 
have  only  recently  recovered  from  heart  failure,  it  is  a  safe  rule  to  in- 
terdict marriage  until  at  least  two  years  have  passed  without  further 
break  in  compensation.  An  exception  is  noted  later  in  reference  to  aortic 
lesions  and  extreme  cardiac  hypertrophy.  The  interval  mentioned  — 
two  years  —  is  of  course  purely  arbitrary,  but  seems  to  agree  best 
with  clinical  experience.  The  same  time  should  be  set  regarding  the 
interval  of  freedom  from  inflammation  in  valvular  lesions.  If,  for 
example,  there  have  been  rheumatic  endocarditic  recrudescences,  as 
shown  by  louder  murmurs,  slight  febrile  attacks,  pericarditis,  tachycardia, 
arrhythmias,  or  other  clinical  manifestations,  marriage  should  not  be 
advised,  for  the  chances  are  that  another  outbreak  will  occur  before 
one  year  has  passed.  In  short,  marriage  (and  pregnancy)  may  be 
considered  safe  if  excellent  compensation  and  freedom  from  endocardial 
exacerbations  persist  during  the  two-year  period.  The  physician  who  has 
not  had  the  opportunity  to  observe  the  patient  within  the  prescribed 
antenuptial  period  must  necessarily  be  guided  by  the  history  and  the 
physical  signs. 

Of  the  two  factors,  decompensation  and  quiescence  of  the  lesion, 
I  believe  that  the  latter  is  the  more  important.  In  my  experience, 
more  danger  and  more  fatalities  have  resulted  in  subsequent  preg- 
nancies from  marriage  occurring  when  lesions  were  active  than  from 
mild  decompensation.  Pregnancy  seems  to  light  up  dormant  or  only 
partially  active  cardiac  processes.  Cardiac  symptoms  often  begin 
early,  sometimes  in  the  third  month  of  pregnancy.  At  the  beginning, 
simple  or  paroxysmal  tachycardia  may  be  present.  Slight  fever  may 
appear;  when  due  to  endocardial  exacerbations,  its  presence  is  of 
serious  import.  The  occurrence  of  new  or  louder  valvular  murmurs, 
or  of  fresh  pericarditis,  may  also  furnish  direct  evidence  of  inflammatory 
recrudescence.  Hemoptysis  is  not  infrequent.  As  pregnancy  advances, 
unless  the  above  or  similar  manifestations  recede  or  are  checked,  dysp- 
noea and  cyanosis  gradually  supervene  and,  with  them,  the  usual 
symptomatology  of  frank  cardiac  decompensation :  edema,  orthopncea, 
enlarged  liver,   pulmonary  congestion,   etc.     The  greater  circulatory 


MANAGEMENT   OF   CARDIAC   DISEASE  239 

demands  made  by  the  growing  placental  and  foetal  circulation  also 
play  a  role,  in  all  probability.  Labor,  induced  or  spontaneous,  does 
not  always  terminate  the  circulatory  embarrassment,  for  insidious 
endocarditis  may  continue,  and  death  result  from  some  complication 
or  from  circulatory  failure. 

Fundamental  considerations  which  refer  to  all  types  of  valvular 
lesions  with  reference  to  marriage  have  already  been  mentioned.  It 
now  remains  to  partially  differentiate  between  these  upon  the  basis 
of  clinical  experience.  I  have  found  that  rheumatic  mitral  stenotic 
lesions  are  the  most  dangerous  to  pregnant  women.  These  patients 
readily  develop  paroxysmal  or,  more  often,  simple  tachycardia,  which  may 
last  during  the  greater  part  of  pregnancy.  The  rapid  heart  action  itself 
may  produce  such  dyspnoea  or  discomfort  that  the  induction  of  pre- 
mature labor  is  indicated.  Hemoptyses  are  common.  Bronchitis 
with  sibilant  breathing  and  mucous  rales  over  the  entire  chest  are  not 
unusual.  As  occasional  complications  in  the  puerperium,  embolic 
infarcts  in  the  lower  extremities  or  in  the  lungs  may  be  mentioned. 

The  history  of  pregnant  women  with  mitral  stenosis  and  auricular 
fibrillation  presents  a  varied  clinical  picture.  Some  of  these  patients 
date  their  first  break  of  compensation  at  a  first  or  second  pregnancy 
which  had  been  carried  to  full  term.  On  the  other  hand,  I  have  observed 
cases  who  went  through  successive  pregnancies  with  mitral  stenosis 
and  auricular  fibrillation,  with  no  cardiac  complications  or  symptoms. 
One  of  these  deserves  brief  mention :  When  first  examined,  she  was 
fifty  years  old,  with  general  anasarca,  orthopnoea,  auricular  fibrillation, 
a  double  mitral  lesion,  and  an  old  rheumatic  history.  She  had  had 
eighteen  children  without  cardiac  symptoms.  The  latter  began  only 
three  years  after  her  menopause  which  commenced  five  years  before. 
Another  patient,  fifty-three  years  of  age,  was  the  mother  of  five  children. 
She  had  a  rheumatic  history  and  a  double  mitral  lesion  with  auricular 
fibrillation  for  many  years.  During  her  pregnancies  the  cardiac  symp- 
toms were  very  slight  and  of  the  same  nature  as  those  occurring  when 
she  was  not  pregnant;  these  consisted  in  occasional  dyspnoea  and 
tachycardia. 

There  seems  to  be  no  way  of  determining  in  advance  the  favorable 
or  unfavorable  subjects  for  pregnancy  in  those  with  auricular  fibrilla- 
tion, except  by  the  method  already  outlined.  Extreme  caution  in  ad- 
vising marriage  is,  of  course,  necessary  because  of  the  known  tendency 
of  patients  with  auricular  fibrillation  to  decompensate. 

Patients  with  simple  mitral  regurgitant  lesions  are  most  fit  for  preg- 
nancy and  most  apt  to  go  through  gestation  without  untoward  cardiac 
complications.  When  the  latter  do  occur,  they  are  usually  of  the  mild 
decompensatory  type  rather  than  due  to  recurrence  of  endocardial 
exacerbation. 

Pregnant  women  with  aortic  lesions  suffer  chiefly  from  tachycardia. 
This  is  true  of  those  with,  as  well  as  those  without,  marked  ventricular 


240  CLINICAL  CARDIOLOGY 

hypertrophy.  In  the  latter,  however,  tachycardial  attacks  occur  more 
frequently,  are  more  readily  invoked,  and  of  longer  duration.  De- 
compensation is  comparatively  rare  in  those  with  only  moderate  or 
slight  hypertrophy;  when  extreme,  cardiac  failure  is  apt  to  occur 
early  in  pregnancy,  a  tendency  increased  by  the  rapid  heart  action. 
Such  patients  should  not  be  permitted  to  become  pregnant  even 
if  the  lesion  is  quiescent  and  compensation  in  the  non-pregnant  state 
is  good. 

In  all  types  of  decompensated  endocardial  lesions  occurring  during 
pregnancy  the  question  of  the  induction  of  abortion  or  of  premature 
labor  arises.  Severe  cardiac  failure  in  early  pregnancy  (before  the  fourth 
month)  or  slight  decompensation  which  does  not  yield  to  treatment 
are  absolute  indications  for  immediate  emptying  of  the  uterus.  This 
indication  is  not  vitiated  by  the  fact  that  some  of  these  mothers  may, 
by  protracted  rest  and  medication,  carry  the  child  to  viability  or  even 
to  full  term  without  further  complications.  The  life  of  the  mother  is 
the  prime  consideration  and  should  not  be  jeopardized,  as  it  would  be, 
in  an  attempt  to  continue  the  pregnancy  when  cardiac  decompensation 
is  present  at  an  early  stage.  My  observation  has  been  that  an  abortion, 
surgically  clean  and  skillfully  performed,  is  only  slightly  if  at  all  more 
dangerous  in  cardiac  patients  than  if  performed  for  other  reasons  on 
those  with  normal  hearts.  I  am  also  strongly  in  favor  of  terminating 
an  early  pregnancy  if  it  is  evident  that  there  exists  a  continuance  or 
recrudescence  of  endocarditis.  As  already  indicated,  such  evidence 
may  consist  in  the  onset  of  paroxysmal  or  constant  tachycardia,  of  ex- 
trasystoles  or  other  arrhythmias,  of  frequent  hemoptyses,  and  of  changes 
in  the  physical  signs. 

If  signs  of  decompensation,  or  of  fresh  endocarditis,  appear  between 
the  end  of  the  fourth  month  and  the  time  of  viability  (the  seventh 
month),  in  view  of  the  somewhat  more  serious  operative  procedure 
required  to  induce  miscarriage,  the  decision  regarding  either  procedure 
hinges  chiefly  upon  the  severity  of  the  cardiac  complications.  If  de- 
compensation is  mild  or  the  evidence  of  fresh  endocarditis  not  severe, 
appropriate  therapy  should  at  first  be  attempted  for  about  a  week  or 
ten  days.  Should  the  symptoms  then  disappear  and  the  patient  im- 
prove, pregnancy  may  be  allowed  to  proceed  until  the  period  of  viability. 
If  decompensation  or  endocarditis  do  not  react  well  to  therapy  or  become 
suddenly  severe  and  threatening,  it  is  much  safer  to  induce  miscarriage. 

In  the  interim  between  the  seventh  and  the  ninth  month  of  gesta- 
tion the  decision  regarding  the  interruption  of  pregnancy  in  decom- 
pensated cases  or  in  those  with  recrudescent  endocardial  lesions  is  not 
of  such  vital  importance,  because  the  premature  induction  of  labor 
in  proper  hands  adds  scarcely  any  risks.  The  question  of  waiting  a 
month  or  two  until  a  more  natural  process  of  normal  labor  occurs 
must  depend  upon  the  cardiac  condition ;  that  is,  if  there  is  any  reason 
to  fear  the  slightest  increase  of  cardiac  complications,  it  is  both  wiser 


MANAGEMENT  OF  CARDIAC   DISEASE  241 

and  safer  to  have  pregnancy  terminated  soon  than  to  wait  until  full 
term. 

Aside  from  the  induction  of  abortion  or  of  premature  labor,  the 
treatment  of  the  various  cardiac  symptoms  occurring  during  pregnancy 
is  that  already  described  in  the  chapters  on  endocarditis,  arrhythmias, 
and  cardiac  failure. 

REFERENCES 
Chapter  XVIII 

Barringer,  T.  B.,  Jr.,  and  Teschner,  J. :  The  Treatment  of  Cardiac  Insufficiency, 
etc.,  with  Dumb-bells  and  Bars  ;  Archives  of  Internal  Medicine,  1915,  XVI 
795. 

Graeupner :  Die  funktionelle  Bestimmung,  etc.,  des  Herzmuskels ;  Deutsche 
Med.  Wochenschrift,  1906,  1028. 

Krehl,  L. :   Die  Erkrankungen  des  Herzmuskels,  1913. 

Lewis,  T. :  Observations  upon  Ventricular  Hypertrophy,  etc. ;  Heart,  1913-1914, 
V,  367. 

Moritz  :  EineMethode,  etc.  Orthodiagraphie  ;  Muenchener  Med.  Wochenschrift, 
1900,  XLVII,  992. 

Poyton,  and  Paine  :   Researches  on  Rheumatism. 

Rosenow,  E.  C. :  Etiology  of  Articular  and  Muscular  Rheumatism  ;  Journal  of 
American  Medical  Association,  1913,  LX,  1223. 

Stone,  W.  J. :  The  Differentiation  of  Cerebral  and  Cardiac  Types  of  Hyper- 
arterial  Tension,  etc. ;  Archives  of  Internal  Medicine,  1915,  XVI,  775." 


CHAPTER  XIX 

BLOOD  PRESSURE 

Physiological  Considerations.  —  Blood  pressure  observation  has 
taken  its  place  as  a  routine  method  of  examination  in  clinical  medicine. 
Its  value  and  importance  in  health  and  disease  are  based  upon  the  re- 
sults of  experimental  physiology,  which  demonstrated  that  various 
factors  are  concerned  in  the  estimation  of  blood  pressure.  These  are : 
(1)  Cardiac  Energy;  (2)  Peripheral  Resistance;  (3)  Elasticity  of  the 
Arterial  Wall;  (4)  Volume  of  the  Circulating  Blood;  (5)  Viscosity  of 
the  Blood. 

1 .  Cardiac  Energy.  —  From  the  physical  standpoint,  cardiac  work  de- 
pends upon  the  amount  of  and  velocity  with  which  the  blood  is  pumped 
into  the  arterial  system.  This  in  turn  largely  depends  upon  the  amount 
of  venous  blood  brought  to  the  heart.  If  greatly  diminished,  as,  for 
example,  by  section  of  the  splanchnics,  ventricular  filling  and,  conse- 
quently, systolic  output  are  considerably  diminished.  Other  factors 
being  equal,  an  increased  volumetric  output  raises,  a  decreased  output 
decreases,  the  aortal  pressure.  In  the  normal  animal,  the  pulse  rate 
is  retarded  by  raising  arterial  pressure,  and  accelerated  by  lowering 
it.  This  reaction  does  not  usually  occur  after  vagus  section;  hence 
it  is  probably  due  to  action  upon  the  vagus  center,  partly  reflex  and 
partly  direct.  In  animals,  the  centripetal  nerve  to  this  center  is  the 
depressor  which  sends  terminal  filaments  to  the  ventricular  musculature 
and  probably  also  to  the  aorta.  If  this  nerve  is  cut  or  stimulated  periph- 
erally, it  has  no  effect  upon  the  heart  action  or  blood  pressure.  If 
its  central  end  is  stimulated,  there  is  a  marked  fall  in  blood  pressure 
and  heart  rate.  The  depressor  thus  acts  as  a  defensive  mechanism 
against  unduly  high  blood  pressure.  Its  aortal  filaments  are  stimulated 
by  undue  distention  of  the  vessel. 

2.  Peripheral  Resistance.  —  With  other  factors  unchanged,  the 
blood  pressure  is  increased  with  increased,  decreased  by  lessened  pe- 
ripheral resistance.  The  tension  of  the  normal  artery  depends  upon 
its  tonus,  which  in  turn  chiefly  depends  upon  the  vasomotor  mechanism. 
To  a  lesser  extent,  this  statement  applies  to  some  of  the  veins.  Normal 
tone  is  governed  by  a  proper  balance  between  the  vasodilator  and 
vasoconstrictor  mechanisms,  as  derived  from  the  regulatory  center  in 


BLOOD   PRESSURE  243 

the  medulla.  There  are  other  subsidiary  centers  in  the  spinal  cord ; 
this  is  demonstrated  by  the  fact  that,  after  destruction  of  the  bulbar 
center,  the  arteries  gradually  recover  their  tone.  In  the  experimental 
animal,  general  vasomotor  tone  is  readily  affected  by  distant  and  near 
reflexes.  After  stimulation  of  the  depressor  nerve  the  splanchnic  ves- 
sels become  dilated  and  blood  pressure  falls,  but  stimulation  of  all  the 
other  centripetal  nerves  raises  blood  pressure.  The  abdominal  vessels, 
innervated  by  the  splanchnics,  have  the  greatest  effect  upon  the  general 
blood  pressure  because  they  can  contain  a  large  amount  of  blood  and 
are  easily  influenced  reflexly.  It  is  important  in  this  connection  to 
emphasize  that  reflex  lowering  or  raising  the  blood  pressure  does  not 
simultaneously  affect  vascular  areas  in  the  same  way. 

3.  Elasticity  of  the  Arterial  Wall.  —  Because  of  their  elastic  dis- 
tensibility,  a  large  proportion  of  the  force  of  ventricular  systole  is  stored 
up  in  the  larger  arteries,  which,  by  stretching  and  elastic  recoil,  act  as 
a  reservoir  of  power  after  systole  has  ceased.  By  this  means  the  strain 
of  systole  upon  the  cardiac  musculature,  as  well  as  upon  the  arterial 
wall,  is  considerably  diminished.  If  the  arterial  tree  represented  a 
rigid  system,  the  systolic  blood  pressure,  and  hence  the  force  of  the 
impact,  upon  the  arteries  would  be  greatly  increased. 

4.  Volume  of  the  Circulating  Blood.  —  The  possible  content  of  the 
arterial  and  venous  systems  is  much  larger  than  the  actual  amount  of 
blood  found  in  the  body.  The  disproportion  is  equalized  by  peripheral 
contraction,  hence  blood  volume  has  only  a  very  slight  effect  upon  blood 
pressure. 

5.  Viscosity  of  the  Blood.  —  It  is  evident  that  the  degree  of  vis- 
cosity may  have  some  influence  upon  blood  pressure.  Up  to  the  present 
time,  however,  there  are  no  clinical  or  experimental  data  which  have 
any  bearing  upon  the  subject. 

All  these  factors  are  present  in  the  human  being  as  well  as  in  the 
experimental  animal.  Their  value  and  importance  vary  not  only  rela- 
tively but  absolutely  from  time  to  time,  and  the  blood  pressure  is  the 
resultant  of  these  variants.  Although  we  possess  no  methods  or  instru- 
ments by  which  individual  agencies  making  up  the  clinical  blood  pres- 
sure can  be  separately  calculated,  one  should  at  least  attempt  to  gauge 
them  by  careful  examination  and  by  such  significant  data  as  the  thick- 
ness of  palpable  arteries,  existence  of  plethora,  etc. 

Clinical  Estimation  of  Blood  Pressure. — The  instruments  which  are 
used  in  the  clinical  estimation  of  blood  pressure  are  called  sphygmo- 
manometers and  are  of  two  main  types,  the  mercurial  and  the  aneroid. 
Both  fundamentally  depend  upon  calculating  the  power  exerted  in 
partial  or  complete  obliteration  of  an  artery  in  terms  of  a  column  of 
mercury  or  of  an  aneroid  pressure  indicator,  respectively.  In  its  clinical 
application,  the  brachial  is  the  artery  chosen  for  compression.  This 
is  accomplished  by  means  of  a  standard  12  cm.  broad,  inflatable  cuff 


244  CLINICAL  CARDIOLOGY 

placed  around  the  upper  arm.  To  the  cuff  are  attached  two  tubes : 
one  connected  with  the  small  metal  or  rubber  hand  pump  for  the  pur- 
pose of  inflation,  the  other  connected  with  the  mercurial  column  or  an- 
eroid instrument.  A  disadvantage  of  the  latter  is  that  the  spring  may- 
lose  its  resiliency  and  hence  the  instrument  become  inaccurate.  If 
standardized  sufficiently  often  by  comparison  with  a  mercurial  sphyg- 
momanometer, the  aneroid  manometer  is  as  useful  for  clinical  pur- 
poses as  the  mercurial  instrument.  Its  advantages  are  that  it  is  made 
compactly,  so  as  to  be  more  readily  carried  about,  and  the  dial  can  be 
read  more  conveniently  than  the  millimeter  markings  in  a  column  of 
mercury. 

Arm  cuffs  are  of  two  types :  one,  stiff,  made  of  leather ;  the  other, 
soft  and  made  of  cloth  or  silk.  Though  either  can  be  used,  I  prefer  the 
soft  cuff  because  it  is  pliable  and  more  readily  and  quickly  placed  in 
position. 

Blood  pressure  estimations  of  the  brachial  artery  should  be  taken 
at  the  level  of  the  heart.  For  this  purpose,  the  elbow  of  the  patient 
is  placed  comfortably  upon  a  desk  or  table.  The  cuff  is  then  snugly 
applied  to  the  bare  arm.  The  arm  should  be  relaxed,  otherwise  muscu- 
lar tonicity  tends  to  produce  an  incorrectly  high  blood  pressure  read- 
ing. Edema  also  causes  abnormally  high  blood  pressure,  because  much 
of  the  pressure  within  the  cuff  is  used  up  in  displacing  the  edema. 

The  introduction  and  use  of  the  sphygmomanometer  have  shown  that 
the  estimation  of  blood  pressure  by  radial  palpation  alone  is  erroneous 
and  untrustworthy.  There  are  various  methods  of  determining  the 
systolic  blood  pressure  by  manometric  readings;  these  are  (1)  the 
palpatory,  (2)  the  visual,  (3)  the  graphic,  (4)  the  auscultatory. 

According  to  (1)  the  palpatory  method,  the  systolic  blood  pressure 
is  that  degree  of  cuff  pressure  exerted  on  the  brachial  at  which  the 
radial  pulse  becomes  no  longer  palpable.  (2)  The  visual  method  con- 
sists in  compressing  the  brachial  beyond  the  point  of  obliteration,  and 
then  gradually  lowering  the  pressure  by  cuff  deflation  until  the  first 
mercurial  oscillation  becomes  visible ;  this  point  marks  the  systolic 
blood  pressure.  In  the  (3)  graphic  method,  the  mercurial  manometer 
has  an  additional  connection  with  a  rubber  bulb  inclosed  in  a  her- 
metically sealed  small  glass  globe ;  the  latter  is  attached  to  a  recording 
tambour,  so  that  differences,  as  shown  by  the  mercurial  oscillations,  are 
transmitted  to  the  tambour  and  recorded  on  a  revolving  drum. 

(4)  The  auscultatory  method  is  the  one  usually  employed  because 
of  its  accuracy.  The  cuff  is  applied  and  inflated  until  the  brachial  is 
obliterated,  that  is,  beyond  the  point  at  which  mercurial  oscillations  are 
visible.  The  stethoscope  is  then  applied  to  the  brachial  at  the  bend  of 
the  elbow,  and  the  cuff  is  gradually  deflated  until  sharp  distinct  taps 
are  heard  ;  this  marks  the  systolic  blood  pressure.  In  typical  instances, 
it  is  possible  to  separate  the  auscultatory  phenomena  into  five  distinct 
"  phases."     The  first  is  the  one  just  described  and,  as  noted,  establishes 


BLOOD   PRESSURE  245 

the  systolic  pressure.  The  artery  beneath  the  cuff  being  empty,  the 
first  pulse  wave  produces  sudden  arterial  tension  with  resultant  short, 
popping  sounds.  With  a  gradual  drop  in  blood  pressure  by  continued 
deflation,  the  sharp  tap  gives  way  to  a  murmur,  somewhat  resembling  a 
superficial,  rough  pericardial  friction  sound.  This  marks  the  second 
phase.  It  is  probably  caused  by  sufficient  blood  passing  under  the 
cuff  to  produce  swirling  arterial  currents  which  mask  the  click  of  the 
first  phase.  By  further  deflation  and  consequent  lessened  pressure  on 
the  brachial,  this  murmur  ceases  and  the  third  phase  begins.  It  is 
marked  at  the  beginning  by  short  tapping  sounds  which,  with  continued 
deflation,  gradually  change  to  muffled  taps ;  this  is  usually  regarded  as 
the  beginning  of  the  fourth  phase,  and  as  marking  the  diastolic  pressure. 
Some  dispute  exists  regarding  the  etiology  of  the  sounds  in  the  fourth 
phase.  It  seems  probable  that,  with  the  gradual  approach  of  diastolic 
pressure,  a  steady  arterial  stream  begins  to  flow  beneath  the  cuff  be- 
tween the  arterial  pulsations ;  this  acts  as  a  kind  of  buffer  and  thus  pro- 
duces the  muffled  and  dull  sounds  characteristic  of  the  fourth  phase. 
The  dull  note  is  finally  extinguished  by  a  constantly  increasing  column 
of  blood  in  the  artery,  until  all  sounds  cease.  This  marks  the  fifth  or 
last  auscultatory  phase.  The  usual  difference  between  the  fourth  and 
fifth  phases  is  from  5  to  8  mm.  of  mercury. 

The  various  phases  as  outlined  are  not  always  well  defined  or  dis- 
tinguishable. There  are  several  variations  from  the  normal.  If  the 
brachial  artery  is  small,  the  separate  phases  may  be  indistinct  or  in- 
audible. Again,  the  first  phase  may  not  be  represented  by  a  sharp 
click,  but  by  a  murmur.  Occasionally,  the  second  phase  is  entirely 
absent,  especially  in  aortic  disease  with  high  systolic  blood  pressure. 
Such  differences  probably  depend  upon  the  varying  strength  of  ar- 
terial eddies  interfering  with  the  usual  sharp  taps  of  sudden  arterial 
distention. 

The  maximal  normal  blood  pressure  is  still  a  matter  of  dispute. 
In  a  statistical  table  by  Fisher  representing  19,339  accepted  candi- 
dates for  life  insurance,  including  ages  from  15  to  60,  the  average 
systolic  pressure  was  129  mm.  of  mercury.  As  shown  by  these  and 
other  statistics  and  observations,  it  appears  that  150  mm.  marks  the 
extreme  normal  systolic  blood  pressure  of  a  healthy  middle-aged  indi- 
vidual. The  normal  diastolic  pressure  in  adults  is  from  70  to  90  mm. 
of  mercury.  There  is  a  gradual  rise  in  systolic  and  diastolic  blood  pres- 
sure with  advancing  age. 

There  are  certain  physiological  variations  which  must  be  borne  in 
mind  when  taking  blood  pressure  estimations.  The  systolic  blood 
pressure  is  increased  by  expiration ;  in  forced  expiration  this  may  amount 
to  5  to  10  mm.  There  is  also  a  slight  diurnal  variation  accounted  for 
by  differences  in  physical  and  psychical  states  of  the  individual  at 
various  times  of  the  day.  The  blood  pressure  is  lowest  during  the 
first  part  of  natural  sleep.     The  ingestion  of  meals  has  a  varying  in- 


246  CLINICAL  CARDIOLOGY 

fluence  upon  blood  pressure;  this  depends  upon  different  degrees  of 
vasodilation  of  the  abdominal  vessels  with  compensatory  superficial 
vasoconstriction. 

There  are  certain  factors  which  require  brief  comment  because  of 
their  influence  upon  blood  pressure.  Moderate  amounts  of  alcohol  do 
not  regularly  raise  the  blood  pressure  in  man.  In  the  experimental 
animal,  large  doses  produce  a  fall  in  blood  pressure,  due  to  an  effect  upon 
the  vasoconstrictors  and  upon  the  heart.  When  smoking  tobacco, 
there  is  a  temporary  rise  of  blood  pressure  from  stimulation  of  the 
peripheral  and  central  vasoconstrictor  mechanism.  Excitement  — 
pleasurable  or  otherwise  —  sometimes  produces  a  temporary  rise  of 
blood  pressure.  Exercise  and  muscular  exertion  have  a  similar  effect ; 
in  young  healthy  individuals  the  blood  pressure  soon  drops  to  its  usual 
level ;  in  the  middle-aged  and  old,  the  rise  of  blood  pressure  represents 
a  more  marked  reaction  and  lasts  longer.  Cyanosis  may  in  itself  be 
a  cause  of  abnormally  high  blood  pressure ;  hence  therapeutic  measures, 
like  venesection  and  digitalis  (which  tend  to  diminish  cyanosis),  may 
directly  decrease  existing  hypertension.  This  is  an  important  consider- 
ation in  the  treatment  of  decompensation  and  hypertension  in  which 
cyanosis  forms  an  important  element.  Another  factor  in  the  produc- 
tion of  hypertension  in  some  cases  of  arterial  disease  is  that  due  to 
hypertonus;  this  possible  cause  for  error,  however,  can  be  controlled 
and  obviated  by  repeated  compression  of  the  artery  with  the  cuff. 

In  general,  frequent  blood  pressure  estimations  are  necessary  in 
order  to  arrive  at  the  correct  blood  pressure  of  the  individual,  and  to 
obviate  some  of  the  disturbing  physiological  and  other  factors  that  have 
been  mentioned. 

For  the  purpose  of  studying  abnormal  blood  pressure  in  organic 
cardiovascular  disease,  I  have  found  the  classification  I  devised,  embrac- 
ing the  vast  majority  of  cases,  to  be  of  clinical  value.  Despite  occa- 
sional overlapping,  the  predominant  lesion  or  type  is  usually  readily 
recognized. 

f  (a)  Hypertensive  cardiovascular  disease  with  myocarditis. 
(b)   Hypertension  and  myocardial  insufficiency  with  labile  vasomotor 
mechanism. 
,  (c)    Uremia. 
II.   Myocardial  disease  and  insufficiency  without  hypertension. 

III.  Valvular  disease  and  myocardial  insufficiency  with  and  without  hyperten- 

sion. 

IV.  Senile  and  premature  arteriosclerosis. 

I  (a).  Hypertensive  cardiovascular  disease  with  myocarditis  in- 
cludes some  of  the  fairly  well-defined  groups  of  the  older  writers ;  for 
example,  Huchard's  presclerosis,  Gull  and  Sutton's  arteriocapillary  fibro- 
sis, von  Basch's  angiosclerosis.  It  is  becoming  increasingly  evident 
that  the  pathological  basis  of  hypertensive  cardiovascular  disease  lies 
chiefly  in  disease  affecting  the  arterioles  of  the  heart,  kidneys,  and 


BLOOD   PRESSURE  247 

brain.  As  concomitant  changes  in  the  heart,  there  may  be  cardiac  hy- 
pertrophy (mainly  of  the  left  ventricle)  and  moderate  or  advanced  aor- 
titis. The  systolic  blood  pressure  commonly  varies  from  180  to  230 
mm.  of  mercury,  the  average  being  190  to  200.  It  is  important  to 
note  that  there  may  exist  no  parallelism  between  the  degree  of  hyper- 
tension and  the  extent  of  kidney  involvement,  and  that  hypertension 
alone  need  not  necessarily  be  of  symptomatic  or  prognostic  importance. 
The  average  diastolic  pressure  of  this  group  is  about  100  mm. ;  if  renal 
involvement  predominates,  diastolic  pressures  of  120  or  over  are  found. 

I  (b).  Hypertension  and  Myocardial  Insufficiency  with  Labile  Vaso- 
motor Mechanism.  —  This  group  consists  principally  of  patients  past 
middle  life  with  only  moderate  hypertension  and  wTith  normal  or  mod- 
erately elevated  diastolic  pressure.  The  chief  characteristic  of  the 
blood  pressure  is  its  marked  daily  variation,  being  as  much  as  30  mm. 
of  mercury.  The  symptoms  referable  to  myocardial  insufficiency  are 
mild.  The  patients  are  usually  stout  or  obese  men;  the  prominent 
physical  signs  in  the  chest  are  those  of  bronchitis  and  emphysema.  The 
palpable  arteries  are  not  thickened,  and  nephritic  symptoms  not  marked 
despite  the  presence  of  a  slight  amount  of  albumin  and  of  a  few  casts 
in  the  urine.     Pretibial  edema  is  absent  or  only  very  slight. 

I  (c) .  Uremia.  —  The  cardinal  symptoms  in  patients  of  this  group 
are  headache,  nausea,  vomiting,  varying  grades  of  pallor,  attacks  of 
paroxysmal  dyspnoea,  precordial  distress,  and  nocturnal  polyuria. 
There  are  retinal  changes  of  various  degrees.  The  phenolsulpho- 
phthalein  test  (Chapter  XVII)  shows  diminished  output  in  two  hours, 
the  average  being  between  15  and  30  per  cent.  As  a  result  of  renal  test 
meals  containing  weighed  amounts  of  water,  salt,  carbohydrate,  and 
nitrogenous  constituents  (Chapter  XVII),  and  of  chemical  examination 
of  the  blood,  we  find  as  a  rule  low;,  fixed  specific  gravity  for  the  day  and 
night  urines,  decreased  elimination  of  salt,  water,  and  urea  in  the  urine, 
and  abnormal  amounts  of  non-protein  nitrogen  and  sometimes  of  uric 
acid  in  the  blood.  When  uremic  dyspnoea  is  marked,  there  is  evidence 
of  diminished  blood  alkalinity  (so-called  acidosis).  This  may  be  roughly 
estimated  by  determining  the  amount  of  bicarbonate  of  soda,  admin- 
istered internally,  required  to  render  the  urine  alkaline.  Other  more 
refined  and  direct  methods  consist  in  determining  the  carbon  dioxide 
content  of  the  alveolar  air  by  the  Priestly-Haldane  bag  or  by  the  Fri- 
derica  apparatus,  or  by  testing  the  blood  chemically  according  to  the 
Van  Slyke  method.  It  has  recently  been  emphasized  that  the  differen- 
tiation between  the  "  cardiac  "  and  "  cerebral  "  types  of  hypertension 
can  be  made  by  careful  observation  of  the  diastolic  pressure,  which  pre- 
sumably serves  as  the  better  index  of  the  peripheral  resistance.  The 
diastolic  pressure  is  between  120  and  140  in  the  "  cerebral  "  cases,  i.e. 
in  those  who  suffer  from  such  typical  uremic  signs  as  headache,  vomiting, 
and  retinal  changes ;  it  is  considerably  less  in  those  in  whom  "  cardiac  " 
manifestations  are  especially  prominent. 


248  CLINICAL  CARDIOLOGY 

II.  Myocardial  Disease  and  Insufficiency  without  Hypertension.  — 

Patients  in  whom  myocarditis  is  the  predominant  pathological  condi- 
tion show  little  or  no  hypertension.  The  diastolic  pressure  is  sometimes 
quite  low,  so  that,  even  with  a  normal  systolic,  there  is  an  increase  in 
the  pulse  pressure  and  hence  in  the  cardiac  load. 

III.  Valvular  Disease  with  Myocardial  Insufficiency  with  and  without 
Hypertension.  —  The  valvular  lesions  in  which  the  systolic  blood  pres- 
sure is  high  (without  evidence  of  general  arterial  disease)  are  rheumatic 
affections  of  the  aorta,  especially  aortic  regurgitation.  In  this,  the 
blood  pressure  may  be  between  180  and  200  mm. ;  the  diastolic  pres- 
sure is  abnormally  low,  the  average  being  40  to  25 ;  it  is  occasionally 
zero.  There  thus  exists  a  very  marked  cardiac  overload.  It  has  been 
shown  that,  in  this  valvular  lesion,  the  systolic  blood  pressure  in  the 
femoral  is  often  much  higher  than  in  the  brachial.  This  difference 
I  have  found  to  be  as  high  as  50  mm.  of  mercury  in  individual  instances. 
The  normal  difference  between  leg  and  arm  blood  pressures  is  from  5  to 
10  mm.,  hence  the  diagnostic  importance  of  measuring  the  arm  and 
leg  blood  pressure  in  cases  of  suspected  aortic  regurgitation  in  whom 
such  usual  clinical  signs  as  typical  murmurs  and  the  Corrigan  pulse 
are  absent. 

Unless  arterial  disease  or  cyanosis  is  present,  mitral  lesions  are 
unaccompanied  by  hypertension.  With  beginning  heart  failure,  the 
systolic  blood  pressure  may  become  subnormal.  In  combined  val- 
vular disease  of  the  mitral  and  aortic  valves,  blood  pressure  depends 
upon  the  clinically  predominant  lesion.  For  example,  if  aortic  regur- 
gitation is  the  more  prominent,  the  blood  pressure  will  be  characteristic 
of  that  lesion  ;   if  the  mitral  predominates,  the  pressure  will  be  normal. 

IV.  Senile  and  Premature  Arteriosclerosis.  —  Under  this  caption 
are  grouped  those  cases  with  tortuous  and  thickened  visible  arteries. 
The  heart  valves  and  aorta  present  various  degrees  of  intimal  thick- 
ening and  lime  deposits ;  the  main  coronaries  and  their  branches  are 
thickened,  there  is  marked  myo-fibrosis,  the  heart  may  be  small  or  only 
moderately  enlarged.  Such  patients  often  have  only  slight  hyperten- 
sion or  even  normal  blood  pressure,  unless  renal  involvement  is  clini- 
cally marked. 

In  addition  to  the  foregoing  classified  groups  of  organic  cardio- 
vascular disease,  several  other  important  conditions  which  have  a  direct 
bearing  upon  blood  pressure  estimations  require  brief  description. 

Exophthalmic  Goiter.  —  A  characteristic  of  this  disease  is  the  vari- 
ability of  the  blood  pressure  readings;  there  are  marked  differences 
from  day  to  day.  When  the  disease  is  of  moderate  severity,  hyper- 
tension is  the  rule,  the  range  being  between  160  and  180  mm.  of  mer- 
cury. Extreme  hypertension  without  accompanying  cardiovascular 
disease  is  rare. 

Lead  Poisoning.  —  During  attacks  of  lead  colic  there  is  usually  a 
rise  of  the  systolic  blood  pressure.     This  is  attributable  partly  to  the 


BLOOD   PRESSURE  249 

pain  present  during  the  attack,  but  chiefly  to  the  spasm  of  the  pe- 
ripheral arterioles.  Plumbism  which  causes  disease  of  the  kidneys  and 
arteries,  and  ends  in  nephritis  and  arteriosclerosis  naturally  produces 
hypertension  because  of  the  presence  of  these  lesions. 

Increased  Intracranial  Tension.  —  Hemorrhage,  meningitis,  and 
brain  tumors  are  the  usual  causes  of  this  condition.  As  a  consequence 
of  increased  intracranial  tension,  cerebral  anemia  results,  and  with  it, 
an  increase  —  sometimes  marked  —  of  the  systolic  blood  pressure.  In 
addition  to  the  hypertension,  other  manifestations  of  cerebral  anemia 
may  consist  in  headache,  vomiting,  vertigo,  choked  disk,  and  true 
bradycardia. 

Cyanosis  is  so  frequently  found  in  broken  compensation,  that  its 
effect  in  producing  hypertension  requires  special  consideration.  Its 
action  may  be  ascribed  to  an  effect,  in  a  milder  degree,  similar  to  that 
of  the  blood  in  asphyxia.  In  the  latter  direct  stimulation  of  the  vaso- 
motor center  is  assumed.  Cyanosis  in  itself  may  frequently  account 
for  hypertension  in  decompensation  from  any  cause,  for,  with  de- 
crease of  cyanosis,  the  blood  pressure  often  returns  to  the  normal  and 
remains  there.  Therefore,  by  treating  cyanosis,  diverse  therapeutic 
measures  such  as  digitalis  medication  and  venesection  may  have  a 
direct  and  beneficial  effect  upon  hypertension. 

Functional  Hypertension,  Hyperpiesis.  —  Besides  hypertension  due 
to  known  pathological  change  or  abnormal  clinical  condition,  there 
remains  a  small  group  of  patients  in  whom  at  present  no  cause  for  hy- 
pertension can  be  found.  This  has  been  termed  hyperpiesis.  In  this 
group  may  be  mentioned  females  approaching  the  menopause  and  a  few 
sufferers  from  gastric  disturbances  of  a  neurotic  nature.  The  follow- 
ing is  a  typical  case : 

Female,  age  55,  menopause  8  years  ago.  Some  years  pre- 
viously she  had  gastric  symptoms :  belching,  dizziness,  and  hunger 
pains.  Her  present  complaints  have  lasted  several  months ;  these 
are  dizziness,  slight  nausea,  and  at  times  belching.  Dyspnoea,  edema, 
or  urinary  changes  are  absent;  the  sodium  chloride,  water,  urea  ex- 
cretion, and  sulphophthalein  output  are  normal ;  the  Wassermann 
blood  reaction  is  negative.  The  amount  of  non-protein  nitrogen  in 
the  blood  is  also  normal.  Physical  examination  reveals  no  evidence  of 
cardiovascular  disease.  Despite  all  these  findings  the  systolic  blood 
pressure  is  regularly  about  200,  the  diastolic  normal.  It  is  possible 
that  such  cases  are  referable  to  extreme  susceptibility  of  the  vaso- 
constrictor center  to  reflex  influences.  Until  more  of  these  cases  have 
been  studied  by  means  of  chemical  examination  of  the  blood  and  by  func- 
tional urinary  tests,  and  have  been  followed  to  necropsy,  they  must  for 
the  present  be  provisionally  regarded  as  of  functional,  non-organic 
origin. 

Hypotension.  —  This  term  applies  to  a  group  of  adults  presenting 
no  evidence  of  organic  disease  and  in  whom  the  systolic  blood  pressure 


250  CLINICAL  CARDIOLOGY 

is  about  100  in  males,  90  in  females.  Some  of  these  individuals  are  of 
robust  physique.  They  never  suffer  from  decompensation.  They  often 
run  a  symptomless  course  and  are  then  only  accidentally  discovered  in 
the  course  of  routine  clinical  examinations.  If  symptoms  be  present, 
they  consist  of  rapid  fatigue  following  moderate  exertion ;  the  vasomotor 
system  is  unstable  and  susceptible  to  nervous  influences  of  various  kinds. 
The  patients  flush  or  become  pale  readily.  They  are  excitable,  often 
become  dizzy  or  complain  of  feeling  faint;  indeed,  their  symptoms 
overlap  to  a  great  extent  those  described  under  "  Weak  Heart " 
(Chapter  XX). 

Blood  Pressure  in  Cardiac  Arrhythmias 

It  is  sometimes  important  to  estimate  blood  pressure  when  various 
types  of  pulse  irregularities  are  present.  The  methods  to  be  employed 
in  the  commoner  of  these  require  brief  description. 

Sinus  Arrhythmia  and  Heart  Block.  —  Since  the  beats  at  the  wrist 
are  of  equal  force,  only  the  routine  methods  are  required  for  the  blood 
pressure  determination. 

Alternation.  —  There  is  a  rhythmic  sequence  of  stronger  with  weaker 
beats.  The  systolic  blood  pressure  of  the  stronger  contractions  can  be 
estimated  in  the  usual  manner.  Their  diastolic  pressure  can  thus  also 
be  estimated  if  it  be  higher  than  the  systolic  of  the  smaller  beats.  This 
fact  is  readily  determined  during  the  course  of  the  examination  by  pal- 
pating the  radial ;  the  number  of  radial  beats  which  come  through 
will  then  be  just  half  those  at  the  cardiac  apex. 

Coupled  Rhythm.  —  The  tension  of  the  initial  beats  of  the  couplets 
in  auricular  fibrillation  with  coupled  rhythm  is  not  identical,  but  the 
difference  is  usually  slight,  so  that  for  our  purpose  the  coupling  of 
auricular  fibrillation  may  be  grouped  with  that  occurring  in  extrasy stoles. 
The  systolic  blood  pressure  of  the  initial  stronger  beats  is  calculated 
in  the  usual  fashion.  If  the  diastolic  pressure  of  these  is  greater  than 
the  systolic  pressure  of  the  weaker  contractions  of  the  couplet,  then 
again  the  usual  routine  in  measuring  the  diastolic  pressure  of  the 
stronger  is  followed. 

When  extrasystoles  occur  frequently,  and  at  irregular  intervals,  it  is 
necessary  to  use  a  special  method  similar  to  that  for  auricular  fibrillation 
(q.v.)  in  order  to  estimate  the  systolic  blood  pressure. 

In  auricular  fibrillation  with  gross  irregularity  in  the  force  of  the 
beats,  the  ordinary  routine  cannot  be  applied,  for  it  can  only  estimate 
the  systolic  blood  pressure  of  the  strongest,  and  the  diastolic  of  the 
weakest  beat  at  the  moment  that  the  blood  pressure  is  taken.  When 
all  ventricular  contractions  are  propagated  as  pulse  waves,  and  the 
radial  beats  on  palpation  feel  equal  in  force,  my  observations  have 
shown  that  the  pressures  of  the  individual  beats  do  not  usually 
vary  more  than  10  mm.  of  mercury ;  hence  the  ordinary  method  of 


BLOOD   PRESSURE  251 

estimating  the  systolic  levels  are  sufficiently  accurate  for  clinical 
purposes.  With  extreme  irregularity  in  the  strength  of  the  radial, 
and  with  many  frustrate  and  abortive  beats,  various  methods  have 
been  devised  to  arrive  at  an  approximation  of  the  actual  blood 
pressure.  According  to  one  method,  that  of  James  and  Hart,  the  cuff 
and  stethoscope  are  first  applied  in  the  usual  manner.  These  observers 
have  found  that,  although  the  rate  be  irregular,  the  number  of  ventric- 
ular contractions  for  each  minute  is  approximately  the  same.  Their 
procedure  is  as  follows :  the  number  of  radial  beats  which  pass  under 
the  cuff,  between  pressures  of  150  and  140  mm.  of  mercury,  for 
example,  are  counted,  as  well  as  the  corresponding  number  of  ventricular 
contractions  occurring  during  the  same  time.  The  difference  between 
these  represents  the  number  of  frustrate  or  abortive  beats.  Similar 
observations  are  then  made  for  systolic  blood  pressures  between  140 
and  130,  130  and  120,  etc.,  until  the  systolic  blood  pressure  of  all  the 
beats  which  pass  under  the  cuff  have  been  taken.  The  number  of  pal- 
pable radial  beats  found  at  the  various  blood  pressures  is  multiplied  by 
the  highest  systolic  limit  set  for  that  group ;  these  products  are  added 
and  then  divided  by  the  corresponding  heart  rates  at  the  apex.  The 
result  gives  the  "  average  "  systolic  blood  pressure.  One  objection  to 
the  method  is  that  the  "  average "  includes  many  abortive  beats 
(called  by  the  authors  pulse  deficit)  which  have  no  effect  upon  the  cir- 
culation since  they  propel  no  blood  through  the  arteries.  A  better  and 
more  correct  plan  is  to  "  average  "  the  effective  beats  only,  i.e.  those 
that  actually  have  some  effect  upon  the  circulation  by  the  production 
of  pulse  waves.  This  is  attempted  in  the  "  fractional  "  method  of 
Kilgore,  according  to  which  the  diastolic  pressures  are  also  calculated. 
The  systolic  and  diastolic  pressures  are  plotted  on  a  chart,  the  number 
of  beats  occurring  at  the  various  systolic  and  diastolic  pressures  being 
marked  by  points ;  these  are  then  connected  so  as  to  form  a  smooth 
graph.  In  this  manner  it  is  possible  to  make  fairly  exact  estimations  of 
the  blood  pressure  in  auricular  fibrillation. 


Therapeutics  of  Hypertension 

This  subject  has  been  discussed  in  part  in  a  previous  chapter 
(Chapter  XVI).  Before  remedial  measures  are  considered,  it  is  well 
to  emphasize  that  hypertension  is  almost  always  a  conservative  or 
compensatory  process.  As  a  corollary,  it  follows  that  hypertension 
itself  does  not  necessarily  require  medication,  for  it  is  usually  but 
an  index  of  the  underlying  cardiovascular  or  cardiorenal  mischief. 
It  is  the  latter  which  requires  therapeutic  attack.  Another  im- 
portant consideration  is  that  remedies  acting  upon  the  normal  indi- 
vidual (or  animal)  may  have  an  entirely  different  effect  in  hypertensive 
disease.     This,  I  believe,  is  the  main  reason  for  disappointments  in 


252  CLINICAL   CARDIOLOGY 

the  attempt  to  reduce  blood  pressure  by  vasodilators.  They  have 
been  used  innumerable  times  to  decrease  hypertension,  in  most  cases 
with  no  or  only  slight  temporary  results.  Exceptions  will  be  noted 
later.  Their  inefficacy  should  be  ascribed  to  the  type  of  the  pathological 
change  underlying  hypertension.  For  example,  arterioles  considerably 
thickened  by  disease,  or  in  a  state  of  hypertonus,  can  scarcely  be  influ- 
enced by  drugs  that  exert  their  dilating  power  upon  pliable  arteries  or 
under  normal  conditions  of  nerve  tone. 

In  some  hypertensive  cases,  there  occasionally  occurs  a  temporary 
sharp  rise  of  blood  pressure  beyond  the  usual  level  for  these  individuals. 
This  rise  is  sometimes  marked  by  dyspnoea,  precordial  pain,  headache, 
and  vomiting.  It  is  in  these  that  relief  from  abnormal  hypertension  is 
especially  desirable. 

The  drugs  usually  employed  in  the  reduction  of  blood  pressure  are 
nitrite  of  soda,  amyl  nitrite,  nitroglycerin,  spiritus  setheris  nitrosi, 
erythrol  tetranitrate,  and  mannitol.  In  urgent  cases,  amyl  nitrite 
in  5  minim  pearls  may  be  administered.  Regarding  nitroglycerin, 
the  doses  usually  prescribed,  from  270"  to  y^  of  a  grain  three  times 
daily,  rarely  results  even  in  temporary  blood  pressure  reductions.  If 
its  administration  is  not  followed  by  dizziness,  I  am  in  the  habit  of  pre- 
scribing much  larger  doses,  as  much  as  2V  °^  a  gram  three  times  a  day. 
In  an  experimental  series  of  cases,  for  example,  I  have  given  as  much  as 
^q  of  a  grain  hypodermically.  In  those  with  uremia,  the  effects  upon 
the  blood  pressure  were  disappointing.  Even  these  large  hypodermatic 
doses  only  had  an  occasional  or  temporary  effect  upon  the  blood  pres- 
sure or  symptoms.  In  others  of  this  series,  no  constant  result  following 
nitroglycerin  could  be  determined.  Sodium  nitrite,  when  efficacious, 
seems  to  have  a  more  lasting  effect.  Erythrol  tetranitrate  has  also  been 
used  with  indifferent  results.  I  have  observed  the  best  results  when 
the  vasodilators  were  employed  in  those  individuals  whom  I  have 
grouped  as  "  hypertension  and  myocardial  insufficiency  with  labile 
vasomotor  mechanism  "  (q.v.).  These  patients  are  rarely  uremic;  the 
hypertension  is  relieved  not  only  temporarily  but  sometimes  for  a  pro- 
longed period. 

The  action  of  iodide  of  potash,  a  drug  frequently  prescribed  for  the 
relief  of  hypertension,  is  still  in  dispute.  In  view  of  our  knowledge  that 
syphilis  is  a  frequent  cause  of  cardiovascular  disease,  its  occasional  good 
effects  are  to  be  ascribed,  I  believe,  to  its  action  upon  the  underlying 
luetic  disease. 

Venesection  in  all  cases  of  hypertension  with  urgent  symptoms  is  an 
excellent  temporary  therapeutic  measure,  especially  in  plethoric  and 
cyanotic  patients.  From  400  to  800  c.c.  of  blood  should  be  with- 
drawn. 

Hydrotherapy  —  hot  packs,  oxygen- ,  carbon  dioxide- ,  or  hot  baths, 
or  the  electric  light  bath  —  has  been  advocated  to  reduce  hypertension. 
In  so  far  as  they  promote  diuresis  and  perspiration,  and  thus  rid  the 


BLOOD   PRESSURE  253 

body  of  toxic  material,  they  may  have  some  direct  therapeutic  value. 
Oxygen  and  carbon  dioxide  baths  are  followed  by  varying  and  incon- 
stant effects  upon  the  blood  pressure  (Chapter  XVI).  The  indications 
for  these  gas-impregnated  baths  in  hypertension  depend  upon  the 
degree  of  decompensation,  and,  in  the  main,  follow  those  indications 
already  discussed  for  that  condition.  If  decompensation  is  extreme, 
baths  are  contraindicated ;  if  mild,  and  observation  shows  good  effects 
upon  the  blood  pressure  or  symptoms,  they  may  be  continued.  Even 
in  those  in  whom  there  has  been  a  reduction  of  blood  pressure  in  or 
immediately  following  the  baths,  the  reduction  is  slight  and  transient, 
so  that  the  beneficial  effect  is  probably  to  be  ascribed  to  an  action  upon 
the  general  circulation  rather  than  upon  the  blood  pressure. 

The  effect  of  electric  light  baths,  when  efficacious  in  the  reduction 
of  hypertension,  may  be  ascribed  to  the  heat,  incidental  rest,  and  enforced 
quiet  which  form  part  of  the  treatment. 

Diathermy  —  a  special  application  of  the  D'Arsonval  current  to  the 
precordium  —  is  another  method  employed  as  a  therapeutic  agent  in 
hypertension.  Some  of  the  reports  of  its  effects  ■  are  exceedingly  en- 
thusiastic; claims  are  made,  for  example,  that  hypertension  is  per- 
manently relieved.  In  some  cases  which  I  have  observed,  in  whom  dia- 
thermy was  used  by  other  practitioners,  the  blood  pressure  remained 
at  its  usual  level ;  there  was  no  change  whatever  in  the  symptoms. 

Percussion  over  the  seventh  cervical  vertebra  has  been  used,  the 
object  being  to  exert  a  reflex  influence  upon  the  vasodilators  and  thus 
upon  the  blood  pressure.  The  effect  of  this  procedure  is,  to  say  the 
least,  exceedingly  problematical  and  hypothetical. 

Absence  from  business  and  treatments  at  Spas  have  undoubted 
marked  therapeutic  value  in  many  cases  of  hypertension.  The  reasons 
are  obvious.  Patients  are  away  from  their  ordinary  environment,  their 
routine  of  life  approaches  a  more  normal  and  physiological  standard, 
excitement  and  nervous  tension  become  almost  negligible  factors. 

The  amount  of  exercise  that  should  be  allowed  depends  chiefly  upon 
the  accompanying  cardiovascular  disease  and  upon  the  symptoms,  rather 
than  upon  the  degree  of  hypertension.  At  no  time,  however,  should 
violent  or  fatiguing  exercise  be  permitted.  The  amount  of  rest  is  also 
based  upon  the  same  criteria.  For  example,  an  otherwise  active  busi- 
ness man  still  capable  of  some  physical  exertion,  who  frets  and  becomes 
irritable  when  absolute  rest  is  enjoined,  can  wisely  be  permitted  to  at- 
tend business  for  a  short  period  each  day.  The  week's  work  should  be 
broken  by  one  or  two  days  of  rest ;  or  if  the  patient's  condition  allows 
it,  by  mild  exercise  out  of  doors,  especially  walking.  Exercises  of  any 
type  should  be  controlled  by  the  state  and  degree  of  cardiac  compensa- 
tion, and  by  careful  observation  of  the  effect  of  exercise  upon  the  in- 
dividual. 


254  CLINICAL  CARDIOLOGY 

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arterial  Tension,  etc. ;  Archives  of  Internal  Medicine,  1915,  XVI,  775. 
Taussig,  A.  E.,  and  Cook,  J.  E. :  The  Determination  of  the  Diastolic  Pressure 

in  Aortic  Regurgitation ;  Archives  of  Internal  Medicine,  1913,  XI,  547. 
Van  Slyke,  D.  D.,  Cullen,  G.  E.,  and  Stillman,  E. :   Proceedings  of  the  Society 

for  Experimental  Biology  and  Medicine,  1915. 


CHAPTER  XX 
"WEAK"   HEART 

Clinical  Symptoms.  —  "  Weak,"  "  asthenic,"  "  neurotic,"  "  neuras- 
thenic "  hearts  are  some  of  the  terms  more  or  less  loosely  applied  to 
various  ill-defined  conditions  in  which  the  salient  feature  is  an  unstable 
state  of  the  vasomotor  mechanism.  I  shall  not  here  include  a  discussion 
of  the  arrhythmias  which  in  themselves  are  sometimes  regarded  as  evi- 
dence of  a  "  weak  "  heart.  Stress  is  often  laid  upon  the  presence  of 
a  soft,  faint,  systolic  murmur  over  the  apex,  only  slightly  or  not  at  all 
transmitted.  Moderate  hypotension  (Chapter  XIX)  is  also  common 
in  these  individuals.  Unless  one  chooses  to  interpret  such  findings  as 
organic  there  is  no  evidence  of  organic  cardiovascular  disease.  Sub- 
jectively, the  patients  complain  of  tiring  very  easily;  if  the  occasion 
demands  it,  however,  they  can  undergo  long-continued  physical  exer- 
tion with  no  sign  of  strain  upon  the  circulatory  system.  They  also 
often  complain  of  feeling  faint  or  dizzy;  sometimes  they  actually  lose 
consciousness.  Their  faces  and  hands  readily  redden  or  blanch,  with  a 
corresponding  feeling  of  warmth  or  cold  in  these  parts.  These  changes 
are  due  to  vasomotor  instability  and  not  to  "  weak  "  circulation.  This 
is  evidenced  by  the  fact  that  these  patients  never  suffer  from  edema  or 
visceral  congestion,  or  from  any  of  the  signs  found  in  decompensation. 

Aside  from  symptoms  and  physical  signs  referable  to  the  circulation, 
these  individuals  sometimes  suffer  from  ill-defined  gastric  complaints  of 
non-organic  nature  often  associated  with  referred  intercostal  and  pre- 
cordial pains.  It  is  because  of  these  that  one's  attention  is  drawn 
to  the  heart  as  the  presumed  offending  organ.  Nervous  strain,  joy, 
worry,  excitement,  and  physical  fatigue  quickly  elicit  many  of  these 
symptoms  I  have  referred  to.  The  same  factors  seem  occasionally  to 
exercise  an  influence  upon  the  apical  murmur,  which,  at  such  times, 
becomes  somewhat  louder.  The  cause  of  this  increased  intensity  is 
not  clear;  it  may  consist  in  some  disturbance  of  the  muscular  ring 
at  the  mitral  opening,  allowing  regurgitation. 

These  patients  are  as  a  class  usually  regarded  as  neurasthenic, 
because,  though  frequently  of  robust  appearance,  little  or  no  physical 
basis  for  their  symptoms  can  be  found.     Many  have  been  fluoroscoped 

255 


256  CLINICAL  CARDIOLOGY 

in  a  search  for  some  abnormality  in  the  size  and  shape  of  the  heart 
in  order  to  account  for  the  instability  of  the  circulation.  "  Drop  " 
hearts  (Chapter  IX)  and  abnormally  small  hearts  (so-called  microcardia) 
have  been  found  in  some  of  these  individuals.  I  have  studied  a  number 
of  cases  of  "  weak  "  hearts  fluoroscopically.  In  some  I  have  found  the 
abnormal  orthodiascopic  types  above  referred  to;  in  others,  I  have 
found  the  heart  of  normal  size  and  contour,  or  with  the  left  ventricle 
lying  quite  broad  and  flat  upon  the  diaphragm.  In  other  words,  there 
was  no  orthodiascopic  picture  that  I  observed  to  be  definitely  correlated 
with  "  weak  "  heart.  In  addition,  I  have  made  the  fluoroscopic  observa- 
tion that  some  of  these  "  weak-hearted  "  individuals  show  particularly 
vigorous  and  strong  ventricular  contractions.  It  is  therefore  clearly 
evident  that  there  is  no  constant  parallelism  between  the  vasomotor 
symptoms  and  the  muscular  power  of  the  heart. 

A  few  brief  illustrative  clinical  histories  and  findings  will  serve 
to  typify  some  of  these  patients. 

A  buxom  woman  of  45  had  been  told  for  years  that  her  heart  was 
'  weak.'  There  was  no  history  of  any  previous  serious  illness.  She  had 
had  two  children  who  died.  Very  soon  after  the  death  of  the  last  child, 
there  began  a  series  of  symptoms  consisting  of  giddiness,  nausea,  and 
flushing  or  pallor  of  the  face.  These  symptoms  have  been  intensified  since 
her  menopause  two  years  ago,  so  that,  in  addition,  she  often  feels  faint 
and,  in  fact,  actually  fainted  several  times.  There  is  a  very  soft  systolic 
murmur  at  the  apex,  the  orthodiascopic  tracing  shows  an  outline  slightly 
broader  than  the  normal,  the  blood  pressure  and  all  the  other  physical 
findings  are  normal.  This  patient  has  been  under  my  observation  for 
several  years.  She  has  undergone  a  severe  operation  for  appendicitis 
with  no  effect  upon  her  circulation. 

A  vigorous  woman  of  40,  married  and  the  mother  of  two  children, 
while  abroad  was  suddenly  called  home  by  illness  in  her  family.  She 
became  worried,  and  soon  complained  of  feeling  fatigued ;  her  hands 
and  face  readily  became  cold;  she  had  pains  across  the  chest  upon 
exertion.  There  was  a  faint  systolic  murmur  at  the  apex ;  orthodiascopic 
examination  revealed  a  somewhat  broad  left  ventricle;  otherwise  the 
cardiovascular  and  general  examination  revealed  nothing  abnormal. 
Upon  being  assured  that  her  heart  and  other  organs  were  normal, 
she  soon  recovered  her  mental  poise.  She  began  taking  active  exercise 
and  now  walks  several  miles  daily  without  cardiac  or  other  com- 
plaints. 

A  tall,  narrow-chested,  and  somewhat  anemic  youth  of  20  complained 
of  frequent  flushes  and  a  feeling  of  "  heat "  in  the  face.  The  lungs 
and  cardiovascular  system  were  normal.  The  only  abnormal  finding 
was  a  narrow  and  pendulous  heart.  Upon  being  told  after  the  examina- 
tion that  there  was  no  lesion  of  any  kind  in  the  heart  and  lungs,  he  began 
leading  a  more  normal  and  athletic  life  with  rapid  disappearance  of  the 
vasomotor  symptoms. 


"WEAK"  HEART  257 

I  believe  it  is  worth  while  emphasizing  that  the  fundamental  ab- 
normality of  this  entire  group  of  patients  lies  in  an  instability  of  the 
vasomotor  mechanism,  the  cause  of  the  irregular  flushes,  pallor,  dizziness, 
and  faintness.  ,  Nerve  shock  of  any  kind  is  often  the  culminating 
factor  initiating  the  more  acute  symptoms. 

To  a  great  extent,  therapy  lies  in  firmly  assuring  the  patient  that 
there  is  no  organic  disease,  and  that  the  symptoms  can  be  cured  or  at 
least  greatly  alleviated.  It  is  a  diagnostic  and  therapeutic  error  to 
dismiss  these  individuals  by  telling  them  that  they  are  "  nervous," 
for  the  symptoms  are  real  and  usually  beyond  their  control.  The 
treatment  sometimes  requires  patience  and  always  careful  individuali- 
zation. The  patient  should  never  follow  any  form  of  exercise,  no 
matter  how  slight,  to  the  point  of  fatigue.  If  no  improvement  follows, 
a  rest  cure  for  a  longer  or  shorter  time  may  be  required.  Patients 
too  intent  upon  business  must  decrease  the  number  of  hours  and  the 
intensity  of  their  work.  At  no  time  should  these  individuals  feel  hurried 
at  their  work  or  even  at  their  pleasures.  Rest  in  the  reclining  position, 
getting  up  late,  having  breakfast  in  bed,  long  rest  at  night,  mild  balneo- 
therapy; later,  graded  calisthenics,  or  exercise  in  the  open  (golfing, 
tennis,  swimming),  are  measures  which,  appropriately  applied  and 
carefully  selected,  are  of  great  aid  to  the  patient  in  helping  him  regain 
his  vasomotor  equilibrium  and  in  finally  enabling  him  gradually  to 
return  to  his  accustomed  duties. 

Among  drugs,  I  have  found  a  combination  of  atropine  sulphate 
(grains  ^  to  yfo)  with  nitroglycerin  (grain  T£g  to  to).  ,  three 
times  a  day  before  meals,  of  most  value.  Where  hypotension  is 
present,  suprarenal  extract  is  sometimes  of  value.  In  addition,  strych- 
nine may  be  helpful.  If  symptoms  are  intensified  at  menopause, 
ovarian  extract  (corpus  luteum)  may  be  tried.  It  must  be  stated, 
however,  that  because  of  the  type  of  the  fundamental  disorder  —  in- 
stability of  the  vasomotor  mechanism  —  the  effect  of  treatment  is 
sometimes  disappointing  to  the  physician  and  discouraging  to  the 
patient. 

REFERENCES 
Chapter  XX 

Adler  and  Krehbiel :  Orthodiascope  Observations  concerning  a  Certain  Type 
of  Small  Heart,  etc. ;  Archives  of  Internal  Medicine,  1912,  IX,  346. 

DaCosta,  J.  M. :  On  Strain  and  Overaction  of  the  Heart ;  Third  Toner  Lecture, 
May,  1874. 

DaCosta,  J.  M. :  Cardiac  Asthenia  or  Heart  Exhaustion ;  American  Journal  of 
the  Medical  Sciences,  1894,  CVII,  361. 


CHAPTER  XXI 

PRECORDIAL     PAINS     OF     CARDIOVASCULAR     AND     OF 
EXTRACARDIAC   ORIGIN  —  ANGINA  PECTORIS 

Historical.  —  As  early  as  1772,  Heberden  described  angina  pectoris. 
Nothnagel  ascribed  it  to  spasm  of  the  coronaries,  with  consequent 
local  ischemic  and  nutritive  changes  in  the  musculature,  a  theory  which 
has  profoundly  affected  the  literature  of  the  subject.  Huchard  divided 
angina  pectoris  into  true  and  false :  that  produced  by  effort  he  called 
true,  that  without  effort,  false  angina.  Mackenzie  ascribed  the  fun- 
damental cause  of  cardiac  pains,  a  term  which  he  prefers  to  angina,  to 
exhaustion  of  the  cardiac  musculature.  Osier  described  four  types 
of  angina  pectoris :  the  reflex,  neurasthenic,  hysterical,  and  the  Noth- 
nagel. 

Confusion  of  Terms. — The  frequent  indiscriminate  use  of  such  terms 
as  "  false  angina  pectoris,"  "  angina  sine  dolore,"  "  angina  vasomotoria," 
"  angina  vera,"  etc.,  with  no  clear  sense  of  their  etiology  or  pathology, 
has  added  to  the  difficulty  of  comprehending  the  fundamental  causes 
of  precordial  pains.  This  confusion  in  symptomatology  and  pathology, 
and  the  fact  that  precordial  pains  of  similar  distribution  and  character 
may  be  caused  both  by  intra-  and  extracardiac  disease,  have  led  me  to 
make  a  careful  study  of  those  patients  in  whom  these  pains,  from  what- 
ever cause,  were  the  only  or  the  most  prominent  symptoms.  It  appears 
to  me  that  the  term  "  precordial  pain  "  obviates  much  of  the  confusion 
of  the  nomenclature,  and,  when  etiologically  defined,  gives  rise  to  a 
fairly  clear  clinical  conception  of  the  underlying  cardiovascular  or  other 
disease.  In  every  case  that  I  studied,  a  very  careful  history  (the  im- 
portance of  which  is  often  overlooked)  was  obtained.  Besides  the 
routine,  the  clinical  examination  often  included  phenolsulphonephthal- 
ein  and  sodium  chloride  excretion  tests,  chemical  examination  of  the 
blood,  and  electrocardiographic  and  orthodiascopic  tracings.  The  type, 
character,  intensity,  and  distribution  of  the  pain,  the  time  of  its  ap- 
pearance, its  correlation  with  exercise,  with  digestive  or  other  dis- 
turbances, and  the  presence  or  absence  of  Head's  zones,  were  noted. 
After  study  of  all  data,  an  attempt  was  made  to  discover  the  probable 
fundamental  etiologic  lesion  in  the  cardiovascular  system  (myocardium, 

258 


PRECORDIAL  PAINS  259 

endocardium,  kidneys,  or  arteries),  or  in  a  distant  organ  (usually  the 
gastro-intestinal  canal),  and  to  gauge  the  extent  and  severity  of  the 
pathologic  damage  to  be  therapeutically  attacked.  In  this  manner, 
besides  obtaining  a  rational  view  of  the  entire  subject,  one  could  fairly 
definitely  pick  out  and  group  patients  in  whom  therapy  would  be  of  no 
avail,  as  well  as  those  in  whom  it  perhaps  offered  a  good  outlook  ior 
relief  or  even  symptomatic  cure. 

Studies  of  the  cardiovascular  nerve  supply  have  shown  that  there 
are  rich  ganglionic  and  nerve  plexuses  which  surround  the  heart  and 
the  root  of  the  aorta  (Chapter  I)  and  which  are  formed  by  branches 
of  the  vagus  and  sympathetic.  There  are  also  ganglionic  cells  and 
nerve  fibrils  in  the  sino-auricular  node,  the  auriculo-ventricular 
bundle,  and  throughout  the  cardiac  musculature  (Chapter  II).  So 
far  as  known,  nerves  of  sensation  are  absent.  Through  the  funda- 
mental work  of  Sherrington,  Head,  and,  later,  of  Mackenzie,  it  is 
known  that  a  viscus,  though  not  possessed  of  nerves  of  sensibility, 
may,  when  irritated,  excite  the  corresponding  visceral  segment  of 
the  spinal  cord ;  the  latter  then  sends  abnormal  centrifugal  impulses 
to  the  muscles,  glands,  etc.,  which  in  the  skin  give  rise  to  abnormal 
sensations  usually  felt  and  denoted  as  pain.  In  cardiac  disease  the 
area  ordinarily  affected  is  the  precordium.  Depending  upon  the 
nerves  involved,  the  intensity  of  the  irritation,  or  possibly  upon 
irradiation  of  centripetal  impulses  to  other  spinal  segments,  pain 
may  spread  to  the  entire  chest,  to  both  arms  (especially  the  left),  the 
fingers,  neck,  head,  the  interscapular  region,  the  epigastrium,  the  ab- 
domen, and  even  the  thighs.  Besides  the  precordium  and  left  shoulder, 
the  epigastrium  is  the  favorite  site  for  referred  pains,  a  fact  which  often 
causes  erroneous  diagnoses,  and  mistakenly  directs  the  therapy  to  the 
stomach.  In  severe  cases,  pain  is  usually  sharp,  lancinating  or  agonizing 
in  character,  and  combined  with  the  oft-described  feeling  of  impending 
death.  In  milder  cases,  it  is  dull  or  aching,  or  there  may  be  merely  a 
feeling  of  oppression  on  the  chest.  Head's  zones  are  sometimes  present, 
usually  over  the  precordium,  more  rarely  in  the  epigastrium.  Occa- 
sionally the  pressure  even  of  wearing  apparel  produces  severe  pain.  The 
sensitiveness  may  be  confined  to  the  underlying  intercostal  muscles; 
deep  pressure  alone  then  elicits  pain.  It  is  sometimes  possible  in  a 
general  way  to  judge  of  the  effect  of  therapy  and  of  the  progress  of  the 
disease  by  the  amount  of  pain  elicited  upon  superficial  or  deep  pres- 
sure ;  when  the  progress  is  favorable,  sensitiveness  to  pressure  dimin- 
ishes. 

In  this  connection  it  is  important  to  discuss  the  frequency  of  epi- 
gastric pains  and  of  occasional  epigastric  Head's  zones  found  in  heart 
disease.  The  former  are  usually  ascribed  to  an  enlarged  liver  or  to 
congested  gastric  mucous  membrane.  However,  the  pains  are  present 
when  the  liver  is  not  enlarged,  and  necropsy  reports  show  that  such 
patients  often  had  no  congestion  or  disease  of  the  gastric  mucosa.     Be- 


260  CLINICAL  CARDIOLOGY 

sides,  we  possess  no  data  which  definitely  correlate  such  presumed  con- 
gestion with  pain.  From  clinical  manifestations,  from  disappearance  of 
epigastric  tenderness  pari  passu  with  decompensation,  and  from  the 
intimate  correlation  of  the  nerve  supply  of  stomach  and  heart,  it  seems 
probable  that  this  type  of  pain  is  chiefly,  if  not  entirely,  the  result  of 
referred  nerve  excitation  from  cardiac  disease. 

Clinically  and  etiologically,  precordial  pain  is  divided  into  that  due 
to  intracardiac  and  to  extracardiac  disease.  This  distinction  is  at 
times  difficult  or  even  impossible,  but  the  attempt  at  differentiation 
is  of  fundamental  importance.  For  the  purpose  of  clinical  classifica- 
tion, the  term  "  myocardial  insufficiency  "  is  here  used  as  equivalent  to 
cardiac  failure  or  incompetency. 

Commoner  Causes  of  Precordial  Pain.  —  The  subject  will  be  con- 
sidered according  to  this  outline x : 

A.  Organic  cardiovascular  disease  : 

1.  (a)  Hypertensive    cardiovascular    disease    with    myocardial    in- 

sufficiency.    (6)  Hypertension  and  myocardial  insufficiency 
with  labile  vasomotor  mechanism,      (c)  Uremic  group. 

2.  Myocardial  insufficiency  without  hypertension. 

3.  Acute    rheumatic    endocarditis    and    rheumatic    endocarditic    ex- 

acerbations. 

4.  Endo-myocardial  disease  with  general  circulatory  failure. 

5.  Embolic  infarcts  in  the  main  coronaries  and  their  branches. 

6.  Cardiac  syphilis. 

7.  Premature  arteriosclerosis  and  cardiosclerosis. 

8.  Senile  arteriosclerosis  and  cardiosclerosis. 

9.  Sacculated  aneurism. 
10.    Tabagism  (?). 

B.  Extracardiac  disease : 

1.  Gastro-intestinal  disease  (organic  and  functional). 

2.  Esophageal  disease  (organic  and  functional). 

3.  Crises  of  catarrhal  pulmonary  affections. 

4.  Vasomotor  disturbances  at  the  menopause. 

5.  Neuralgias  (?)  of  unknown  origin. 

6.  New  growths  and  disease  of  the  mediastinum,  spinal  cord  and  bony 

structures   of   the   chest ;    intercostal   myalgia   and    neuralgia ; 
pericarditis. 


A.   Precordial  Pains  Due  to  Organic   Cardiovascular  Disease 

1.  (a)  Hypertensive  Cardiovascular  Disease  with  Myocardial  Insuffi- 
ciency. —  The  patients  of  this  group  probably  represent  the  most  fre- 
quent sufferers  from  precordial  pains.  The  cause  of  hypertension  has  been 
ascribed  by  some  to  an  increase  of  epinephrin  in  the  blood,  though  care- 
ful experiments  by  Janeway  and  Park  have  not  justified  this  assump- 
tion. Recent  studies  of  blood  metabolism  have  shown  that  chronic 
nephritis  with  hypertension  is  often  accompanied  by  an  increased  amount 
of  non-protein  nitrogen  in  the  blood,  and  by  a  diminution  of  blood 

1  Some  of  these  groups  have  already  been  discussed  in  the  chapter  on  Blood 
Pressure  (Chapter  XXI)  from  the  hypertensive  standpoint. 


PRECORDIAL  PAINS  261 

i 
alkalinity,  —  facts  which  may  in  the  future  offer  promising  fields  for  ther- 
apy. The  chief  cardiac  changes  are  ventricular  hypertrophy,  usually 
left  but  sometimes  also  right ;  patchy,  fibrous  myocarditis ;  thickened 
aortal  and  mitral  cusps  ;  lime  deposits  on  the  first  portion  of  the  aorta ; 
and  atheroma  and  thickening  of  both  coronaries.  It  must  be  remem- 
bered, however,  that  patients  with  similarly  diseased  hearts  may  have 
little  or  no  precordial  distress. 

A  brief  case  description  will  serve  to  fix  the  type :  a  systolic  blood 
pressure  of  190  mm. ;  a  rough  first  and  a  sharply  accentuated  and 
bell-like  second  sound  at  the  right  base;  evidence  of  marked  left 
ventricular  hypertrophy  with  a  heaving  apical  impulse ;  urine  with 
or  without  albumin  or  casts  ;  very  slight  pretibial  edema  ;  dyspnoea  on 
exertion  or  appearing  suddenly  at  night;  nycturia.  The  pains  are 
usually  dull,  most  marked  in  the  precordium,  and  radiate  to  the  neck 
and  arms. 

Almost  frantic  therapeutic  efforts  are  made,  as  a  rule,  to  reduce  the 
high  blood  pressure,  wThile  the  fact  that  it  is  often  a  conservative;  com- 
pensatory process  seems  to  be  entirely  ignored.  A  mere  enumeration 
of  the  long  list  of  remedies  is  sufficient  proof  of  their  inadequacy.  Vaso- 
dilators (nitroglycerin,  amyl  nitrite,  erythrol  tetranitrate),  hot,  Nau- 
heim,  and  oxygen  baths,  violet  ray,  diathermy,  and  electric  light  baths 
are  the  most  popular.  There  are  conflicting  and  contradictory  reports 
regarding  all.  In  some  cases,  as  already  remarked  (Chapter  XIX),  I 
studied  the  effects  of  hypodermic  injections  of  1  per  cent  solutions  of 
nitroglycerin  in  doses  of  one  tenth  grain,  three  times  a  day,  with  no 
effect  on  the  symptoms  and  only  occasional  temporary  reduction  of  the 
blood  pressure.  The  physical  changes  in  the  coronaries  probably  ac- 
count for  the  futility  of  vasodilators  to  regulate  the  impoverished 
cardiac  circulation  and  to  relieve  the  resultant  precordial  symptoms. 
While  theories  such  as  cardiac  spasm  and  anemia  have  had  vogue  as 
the  causes  of  the  pain,  it  seems  more  probable  that  the  underlying 
factor  is  nutritional  cardiac  disturbance  either  from  inadequate  coronary 
circulation  or,  possibly,  from  toxic  products  flowing  in  the  general 
circulation.  Acute  violent  pains  call  for  morphine.  Pearls  of  nitrite 
of  amyl  may  also  be  of  aid.  With  milder  symptoms,  nitroglycerin 
occasionally  gives  some  relief,  especially  if  combined  with  atropine 
sulphate.  Aside  from  temporary  therapeutic  measures,  I  have  placed 
main  reliance  on  digitalis,  either  digipuratum,  or  the  tincture  in  15- 
drop  doses,  three  times  a  day.  The  drug  should  be  given  whether  the 
auricles  fibrillate  or  the  pulse  is  rhythmic,  and  should  not  be  stopped 
when  pains  and  other  symptoms  improve,  but  continued  in  smaller 
doses  for  a  long  period.  A  curb  should  be  put  on  the  patient's  physical 
activity.  Mental  excitement  and  stress  should  be  avoided.  The 
theoretical  objection  that  digitalis  may  perhaps  cause  or  increase  cor- 
onary spasm  has  not  been  verified  by  clinical  evidence  in  cases  in  which 
the  drug  had  been  given  for  months.     In  only  one  of  my  cases  were 


262  CLINICAL  CARDIOLOGY 

precordial  pains  increased  by  digitalis,  although  even  here  there  was 
improvement  for  several  months. 

The  importance  of  treatment  of  edema  and  other  manifestations  of 
cardiovascular  disease  lies  in  their  fundamental  association  with  pre- 
cordial pains.     This  is  illustrated  in  the  following  case : 

A  vigorous  woman  of  43,  never  pregnant,  complained  for  three  years 
of  dyspnoea  on  walking,  and  stabbing  precordial  pains  radiating  to  the 
left  shoulder.  The  Wassermann  blood  reaction  was  negative.  The 
urine  contained  a  trace  of  albumin  and,  occasionally,  hyaline  casts. 
There  was  slight  pretibial  edema.  Physical  examination  revealed  typ- 
ical signs  of  aortitis.  The  orthodiascopic  tracing  showed  an  enlarged 
left  ventricle  and  a  dilated  aortal  arch.  The  precordial  area  was  tender 
to  deep  pressure.  The  lowest  systolic  blood  pressure  was  175  mm., 
the  highest,  220  mm.  There  has  never  been  any  correlation  between 
the  symptoms  and  blood  pressure.  For  the  first  few  months  she  was 
put  on  digitalis,  theobromin  sodium  salicylate,  and  occasional  Karrell 
days.  Within  two  months  the  cardiac  pains  and  pretibial  edema  dis- 
appeared. Later,  when  remiss  in  taking  medication  and  diet,  dyspnoea 
and  pain  recurred.  Under  stricter  surveillance,  and  the  same  medication 
combined  with  absolute  rest  at  home  on  the  Karrell  days,  twice  weekly, 
she  again  slowly  improved.  This  plan  of  treatment  has  been  followed 
for  three  years.  The  blood  pressure  is  still  high;  data  revealed  by 
physical  and  roentgen  examination  are  the  same,  but  there  is  very 
marked  clinical  improvement;  precordial  pains  and  edema  have  en- 
tirely, and  the  dyspnoea  almost  entirely,  disappeared. 

(6)  Hypertension  and  Myocardial  Insufficiency  with  Labile  Vaso- 
motor Mechanism.  —  In  a  smaller  group  of  cases,  in  which  the  high- 
est systolic  blood  pressure  was  around  180  mm.,  with  marked  diurnal 
variations  of  as  much  as  30  mm.,  precordial  pains  following  exercise 
were  the  main  symptoms.  Nephritis  was  apparently  not  the  main  or 
the  only  cause  of  hypertension ;  emphysema  and  myocarditis  were  the 
chief  pathologic  conditions.  Experimental  subcutaneous  injections  of 
nitroglycerin  in  doses  of  one  fiftieth  grain  three  times  a  day  had  a 
marked  temporary  effect  on  the  blood  pressure,  and,  usually,  on  the 
symptoms ;  in  one  instance,  the  injections  were  regularly  accompanied 
by  sudden  relief  of  precordial  pains  to  be  followed  by  giddiness.  Such 
cases  apparently  represent  examples  of  disturbed  labile  vasomotor 
mechanism  rather  than  hypertension  due  to  marked  vascular  disease. 
Nitroglycerin  or  other  vasodilators  given  at  the  onset  of  pain  are  apt 
to  be  followed  by  great  relief.  Digitalis,  though  useful,  is  not  as  bene- 
ficial as  in  Group  1. 

(c)  Uremic  Group.  —  Headache,  nausea,  vomiting,  varying  grades 
of  anemia,  attacks  of  paroxysmal  dyspnoea  and  of  precordial  distress, 
high  systolic  and  especially  diastolic  pressure,  nocturnal  polyuria,  and 
changes  in  the  retina,  are  the  cardinal  symptoms.  Kidney  test  meals, 
as  advocated  by  Schlayer  and  others,  usually  show  decreased  salt,  nitro- 


PRECORDIAL  PAINS  263 

gen,  and  water  elimination ;  and  the  blood,  retained  non-protein  nitro- 
gen. The  facial  appearance  in  typical  instances  is  characteristically 
pallid  or  ashy  gray. 

The  precordial  pains  are  not  relieved  by  nitroglycerin,  digitalis, 
or  theobromin  sodium  salicylate.  They  are  apparently  caused  by 
toxic  products  flowing  in  the  general  circulation  and  affecting  cardiac 
nutrition.  Dietetic  measures,  especially  a  diet  low  in  protein  and  rich 
in  carbohydrates,  are  of  most  value.  When  renal  tests  show  no  water 
retention,  ingestion  of  large  quantities  of  fluids  is  sometimes  beneficial. 
For  the  relief  of  pain,  occasional  doses  of  morphine  are  necessary.  On 
the  theory  of  tissue  acidosis,  I  have  tried  the  intravenous  injection  of 
500  c.c.  of  a  5  per  cent  bicarbonate  solution  in. two  cases.  In  one,  there 
was  marked  relief  of  the  precordial  pains  and  other  symptoms ;  in  the 
other,  the  pain  was  relieved  only  for  some  hours.  Glucose  solutions 
given  by  the  Murphy  drip  or  even  intravenously  may  be  of  value. 

2.  Myocardial  Insufficiency  without  Hypertension.  —  The  main 
complaint  of  these  patients,  usually  men  of  sedentary  habits  between 
the  ages  of  50  and  60,  is  slight  precordial  pain  following  exertion.  The 
patients  look  very  well  preserved.  The  urine  is  normal  or  may  con- 
tain a  slight  trace  of  albumin  with  a  few  casts.  Physical  examination 
reveals  a  slight  impurity  of  the  first  sound  at  the  apex,  and  a  soft  sys- 
tolic murmur  at  the  base ;  there  is  no  evidence  of  severe  cardiovascular 
disease.  The  systolic  blood  pressure  is  around  160  mm.,  rarely  much 
higher ;  there  is  no  edema.  The  orthodiascope  tracing  usually  shows 
a  slightly  dilated  aortal  arch  with  the  left  ventricle  lying  broad  and 
flat  on  the  diaphragm ;  it  is  impossible  to  state  if  this  ventricular  con- 
tour is  due  to  flabbiness  or  to  hypertrophy.  It  is  interesting  to  note 
that  these  patients  commonly  give  a  history  of  having  had  painful 
gastric  attacks  in  previous  years,  with  symptoms  pointing  to  gastric 
or  duodenal  ulcer.  Excellent  results  have  followed  the  use  of  digi- 
talis, given  at  first  in  large,  and  then  in  moderate  doses,  and  continued 
intermittently  for  weeks  or  months.  Small  doses  of  atropine  were  some- 
times added.  At  the  beginning,  the  patient's  activity  was  somewhat 
restricted;  later,  moderate  exercise  —  golf  or  walking  —  was  advised. 
Acidulous  food  and  drink  were  interdicted,  and  some  light  form  of 
nourishment  between  meals  was  prescribed.  The  following  is  an  il- 
lustrative case : 

Male,  age  60,  has  for  years  been  careful  about  his  diet,  particularly 
in  the  avoidance  of  acids,  for  indiscretions  were  followed  by  epigastric 
pains.  For  several  months  he  has  complained  of  precordial,  knife- 
like, paroxysmal  pains  on  walking.  Examination  shows  a  well-nour- 
ished man;  there  is  no  edema;  the  urine  contains  no  albumin  or 
casts,  the  average  systolic  blood  pressure  is  160  mm.  The  orthodia- 
scopic  examination  reveals  a  somewhat  enlarged  left  ventricle,  the 
aortal  outline  somewhat  broader  than  normal.  There  is  an  impure 
first  sound  at  the  apex  and  at  the  base.     There  is  no  dyspnoea  or  de- 


264  CLINICAL  CARDIOLOGY 

compensation.  One  digipuratum  tablet  was  given,  at  first  three  times 
daily,  and  then  continued  in  smaller  doses  for  several  months.  Atropine 
sulphate,  T^o  grain,  three  times  a  day,  was  also  prescribed.  The 
patient  is  now  doing  his  regular  work,  has  taken  ocean  baths  during 
the  summer,  and  has  had  no  recurrence  of  precordial  pains. 

3.  Acute  Rheumatic  Endocarditis  and  Rheumatic  Endocarditic 
Exacerbations.  —  These  cases  usually  occur  in  young  persons  with 
definite  rheumatic  histories,  with  mild  tachycardia,  with  no  dyspnoea, 
and  with  marked  auscultatory  evidence  of  valvular  disease  (usually 
mitral  stenosis).  Slight  and  irregular  rise  of  temperature  is  the  rule. 
The  patients  complain  not  only  of  the  subjective  feeling  of  palpitation, 
but  also  of  "  sticking  "  pains  localized  in  the  region  of  the  heart.  There 
are  usually  no  Head's  zones.  The  cause  of  the  rapid  heart  action  and 
of  the  precordial  pains,  even  in  the  absence  of  abnormal  temperature 
and  other  rheumatic  manifestations,  appears  to  lie  in  the  irritative  effect 
of  fresh  exacerbations  of  endocarditis.  The  best  medication  is  sodium 
salicylate  given  in  full  physiologic  doses.  My  routine  has  been  15 
grains  hourly  until  six  doses  have  been  given  or  tinnitus  occurs;  the 
dose  is  then  decreased.  Bromides  in  moderate  amounts,  and  ice  bags 
to  the  precordium,  are  also  helpful.  Comparative  or  absolute  rest  in 
bed  may  be  necessary  for  some  time. 

4.  Endo-myocardial  Disease  with  General  Circulatory  Failure. — 
The  fundamental  cause  of  the  pains  is  apparently  nutritional  disturb- 
ance from  local  circulatory  failure  in  the  heart  itself.  Precordial 
Head's  zones  or  muscle  tenderness  are  often  present.  The  therapy 
for  the  relief  of  pain  is  the  same  as  for  the  decompensation.  This 
ordinarily  means  vigorous  and  long-continued  digitalis  medication, 
and,  for  the  relief  of  edema,  theobromin  and  the  dietetic  regimen  al- 
ready outlined.  If  compensation  is  restored,  cardiac  pains  and  Head's 
zones  disappear. 

5.  Embolic  Infarcts  of  the  Main  Coronaries  and  their  Branches.  — 
It  is  known  that  patients  who  have  recovered  from  cardiac  pains  have 
occasionally  shown  myocardial  scars  and  other  changes  resulting  from 
old  infarcts.  Huchard,  in  a  summary  of  145  necropsies  of  coronary 
disease  with  cardiac  pains,  found  five  due  to  embolism  of  the  artery. 
Recently  several  cases  with  necropsy  reports  of  embolic  infarcts  of  the 
main  coronaries  have  been  described ;  the  patients  died  within  a  few 
days  or  hours  with  symptoms  of  intense  precordial  distress.  I  have 
observed  several  cases  with  intermittent  pains  lasting  days  or  weeks,  in 
which  the  symptoms  were  possibly  caused  by  infarcts  or  emboli  of  the 
smaller  coronary  branches.  Curschmann  in  1891  first  described  this 
condition;  he  reported  three  cases  with  necropsies.  Two  patients 
died  some  years  after  the  onset  of  symptoms.  Both  showed  localized 
myocarditis.  In  one,  there  was  aneurismal  dilatation  confined  to  one 
sclerosed  arteriole;  in  the  other  there  was  an  obliterated  coronary 
branch  of  the  third  order.     The  third  patient,  in  whom  the  condition 


PRECORDIAL  PAINS  265 

was  correctly  diagnosed,  died  suddenly;  an  embolus  was  found  in  a 
coronary  branch  of  the  second  order. 

The  cases  I  observed  are  : 

Female,  unmarried,  aged  18,  under  observation  three  years,  gave  a 
typical  rheumatic  history.  There  is  a  marked  double  aortic  lesion  and 
a  tremendously  hypertrophied  heart.  The  Wassermann  reaction  and 
frequent  blood  cultures  were  negative.  The  systolic  blood  pressure 
was  180  mm.,  the  diastolic,  20  mm.  For  months  she  has  had  many 
attacks  of  moderate  irregular  fever.  On  several  occasions  they  were 
initiated  by  sharp  precordial  pains  followed  by  tachycardia  or  auricular 
fibrillation,  convulsive  twitchings  and  tremors,  and  by  loss  of  con- 
sciousness lasting  several  days.  Latterly  these  attacks  have  become 
more  severe  and  were  followed  by  well-localized  Head's  zones. 

Female,  unmarried,  aged  20,  gave  a  history  of  continued  attacks  of 
rheumatism  and  "  heart  trouble."  During  the  last  few  months  she  had 
two  attacks  similar  to  but  not  quite  so  severe  as  that  with  which  she 
entered  the  hospital.  There  were  continued  agonizing  pains  and 
exquisite  tenderness,  even  to  the  slightest  touch,  over  the  precordium, 
and  radiating  pains  to  the  left  shoulder  and  forearm.  The  temperature 
was  104°.  A  mitral  regurgitant  lesion  was  present.  There  was  no 
edema.  Breathing  was  frequent  and  shallow,  apparently  owing  to  the 
attempt  to  keep  the  chest  at  rest.  After  one  week,  high  temperatures, 
sharp  pain,  and  rapid  breathing  disappeared ;  the  patient  felt  com- 
fortable, but  precordial  pain  on  firm  pressure  was  still  present  when  she 
left  the  hospital. 

Male,  aged  40,  with  a  double  mitral  lesion,  gave  a  history  of  having 
felt  well  until  three  months  prior  to  hospital  admission.  He  then  had 
an  attack  of  mania  (?)  lasting  three  days.  Subsequently  pneumonia 
and  pleurisy  developed,  accompanied  by  chills  and  high  fever,  and  by 
attacks  of  paroxysmal  auricular  fibrillation.  After  several  cultures  a 
non-hemolytic  streptococcus  was  isolated  from  the  blood.  During 
several  months  of  hospital  observation  there  was  a  constant  sensitive 
area  near  the  cardiac  apex. 

The  characteristic  of  these  three  cases  was  not  only  the  rise  of  tem- 
perature and  evidences  of  active  endocarditis,  but  also  the  progressive 
tendency  of  the  disease  and.the  presence  of  local,  tender  precordial  areas. 
Though  these  manifestations  may  have  been  due  to  the  endocarditis 
alone,  the  distinct  localized  sensitive  areas,  and  the  clinical  course,  make 
it  probable  that,  in  addition,  acute  focal  myocarditis  was  present.  From 
clinical  and  physical  signs,  and  from  the  progressive  and  probably  bac- 
terial nature  of  the  endocarditis,  it  seems  fair  to  assume  that  such  focal 
myocardial  changes  originated  in  embolic  infarcts  of  the  smaller  cor- 
onary branches,  accidents  not  necessarily  incompatible  with  life. 

Necropsy  findings  will  of  course  be  necessary  to  establish  the  diag- 
nosis in  such  cases. 


266  CLINICAL   CARDIOLOGY 

6.  Cardiac  syphilis  is  an  extremely  frequent  cause  of  precordial 
pain.  It  is  usually  substernal,  dull,  boring,  and  aching ;  but  may,  how- 
ever, have  the  distribution  and  characteristics  of  the  types  already  de- 
scribed. One  can  probably  ascribe  the  frequency  of  these  substernal 
pains  to  the  almost  invariable  presence  of  syphilitic  aortitis  and  peri- 
aortitis with  consequent  dilatation,  to  the  fact  that  the  root  of  the  aorta 
is  surrounded  by  rich  ganglionic  and  nerve  plexuses,  and  to  the  varying 
degrees  of  aortic  dilatability  and  pressure.  Head's  zones  are  compar- 
atively rare.  Therapy  consists  in  the  treatment  of  the  underlying  dis- 
ease. Although  salvarsan  was  originally  considered  contraindicated  in 
cardiac  syphilis,  abundant  experience  has  since  shown  that,  given  first 
in  smaller,  later  in  larger  doses,  salvarsan  combined  with  the  usual 
mixed  treatment  is  of  great  and  definite  value.  The  best  routine 
method  of  its  administration  is  0.2  gm.  injected  intravenously  every 
week  until  0.6  gm.  is  given;  later,  full  doses  may  be  given,  the  fre- 
quency depending  on  the  cardiac  condition.  Salvarsan  sometimes 
benefits  and  controls  the  pains  immediately,  apparently  because  of 
reduction  in  the  syphilitic  inflammatory  exacerbations.  Where  the 
pathologic  process  in  the  aorta,  the  coronaries,  or  myocardium  has 
reached  an  extreme  degree,  salvarsan  or  any  other  treatment  can  be  of 
little  or  no  avail.  However,  since  our  present  methods  of  examination 
are  not  sufficiently  exact  to  diagnose  such  conditions,  I  believe  the 
treatment  outlined  is  indicated  in  every  case  of  cardiac  syphilis  except 
when  the  patient  is  moribund.  Cardiac  failure,  if  present,  should  re- 
ceive its  appropriate  treatment,  that  is,  digitalis;  and  if  necessary, 
theobromin  sodium  salicylate. 

7.  Premature  Arteriosclerosis.  —  This  comprises  a  rare  group  found 
in  young  adults.  Persistent  precordial  distress  is  often  present  for 
months.  Gastric  symptoms  similar  to  those  of  hyperacidity  occa- 
sionally dominate  the  clinical  picture.  Physical  examination  may  give 
no  hint  of  the  severity  of  the  pathologic  process  attacking  the  entire  car- 
diovascular system,  and  finally  resulting  in  extreme  changes  throughout 
the  aorta,  coronaries,  arterioles,  and  endocardium.  Indeed,  such  hearts 
may  be  pathologically  identical  with  those  of  persons  dying  of  senility. 
For  months  there  may  be  no  decompensation  in  the  ordinary  sense. 
The  urine  may  be  normal,  the  blood  pressure  not  high,  the  heart  sounds 
somewhat  distant,  and  the  only  indication  of  severe  cardiac  disease, 
besides  the  precordial  pains,  may  be  the  presence  of  an  arrhythmia, 
usually  marked  sinus  arrhythmia,  or  extrasystoles.  Other  occasional 
symptoms  are  dyspnoea  and  nocturnal  attacks  of  precordial  distress. 

An  illustrative  case  with  necropsy  report  follows : 

Male,  aged  42,  of  athletic  build,  had  been  a  heavy  smoker.  For  four 
years  he  had  suffered  from  gastric  symptoms  resembling  hyperacidity ; 
belching  was  particularly  prominent.  The  gastric  contents  snowed  high 
values  for  free  hydrochloric  acid.  He  had  frequent  attacks  of  vaso- 
motor disturbances :  numbness,  coldness,  and  pallor  of  the  hands.     It 


PRECORDIAL  PAINS  267 

was  only  late  in  the  disease,  when  an  attack  of  hemiplegia  occurred,  that 
attention  was  focused  on  the  possibility  of  a  generalized  arteriosclerosis 
as  the  underlying  disease.  Although  several  Wassermann  tests  were 
negative,  salvarsan  and  mixed  treatment  were  given ;  these  were  with- 
out effect.  At  necropsy,  marked  thickening  and  calcareous  deposits 
were  found  on  all  the  cardiac  valves ;  the  coronaries  and  their  branches 
showed  extreme  thickening ;  the  myocardium  presented  many  fibrous 
patches ;  the  entire  heart  was  somewhat  enlarged.  Spirochetes  were 
not  found  in  the  aortal  tissue.  The  heart  accurately  resembled  that 
of  a  very  old  person  suffering  for  many  years  from  severe  generalized 
arteriosclerosis  and  cardiosclerosis. 

The  cause  for  such  presenile  sclerosis  is  still  undetermined.  It  is 
possible  that  unknown  infections  and  toxemias  are  etiologic  factors. 
In  one  of  my  patients  the  disease  originated  within  two  years  of  an 
obscure  pulmonary  infection  of  several  months'  duration.  For  the 
present,  one  can  only  state  that,  from  some  unknown  cause,  the  elastic 
tubing  comprising  the  vascular  system  becomes  prematurely  defective 
and  diseased.  Except  digitalis  for  temporary  relief  of  dyspnoea,  treat- 
ment is  of  no  avail. 

8.  Senile  Arterio-  and  Cardiosclerosis.  —  The  clinical  picture  is 
usually  clear.  All  the  palpable  arteries  are  tortuous  and  thickened; 
the  blood  pressure  is  normal  or  not  very  high,  the  heart  somewhat  en- 
larged ;  the  systolic  sounds  at  the  apex  and  right  base  are  impure ; 
the  second  sound  at  the  right  base  is  sometimes  accentuated.  The  pre- 
cordial pains  usually  occur  with  exertion ;  although  sometimes  intense, 
they  are  more  often  of  mild  character.  Apparently  they  basically  de- 
pend on  coronary  sclerosis.  Because  of  the  advanced  pathologic  changes 
the  patients  can  rarely  be  relieved  by  medication.  Digitalis  and  theo- 
bromin  sodium  salicylate  sometimes  help,  the  amount  of  relief  ap- 
parently depending  upon  the  degree  of  healthy  tissue  still  remaining 
to  react  to  medication.  The  patients  usually  require  prolonged  periods 
of  comparative  rest.      % 

9.  Sacculated  Aneurisms.  —  In  a  general  way,  the  precordial  pains 
depend  on  the  size  and  position  of  the  aneurism.  If  large,  the  pains 
are  those  due  to  pressure  on  the  surrounding  structures  (intercostal 
nerves,  ribs,  etc.).  If  small,  and  involving  the  first  portion  or  arch  of 
the  aorta,  the  symptoms  are  similar  in  character  and  etiology  to  those 
described  under  cardiac  syphilis  (Group  6).  The  therapy  is  also  the  same 
as  that  there  indicated.  My  experience  with  wiring  and  the  electric 
current  treatment  according  to  the  method  of  Lusk  is  limited  to  two 
cases.  In  one,  after  some  weeks,  small,  frequent  external  hemorrhages 
occurred,  due  to  the  perforation  of  the  sac  by  the  end  of  the  wire ;  the 
patient  finally  died  of  anemia.  In  the  other,  the  patient  did  not  improve 
during  his  stay  in  the  hospital;  he  died  suddenly  some  weeks  later; 
a  necropsy  was  not  permitted. 


268  CLINICAL  CARDIOLOGY 

10.  Precordial  Pains  Due  to  Tabagism.  —  It  is  questionable  whether 
the  "  tobacco  heart  "  should  be  classified  under  organic  cardiovascular 
disease.  Since  it  has  been  shown  experimentally  that  intravenous  in- 
jections of  nicotine  into  rabbits  are  occasionally  followed  by  aortal 
atheroma,  it  has  by  some  been  assumed  that  smoking  in  man  may  pro- 
duce similar  changes  in  the  vascular  system,  and  possibly  in  the  myo- 
cardium. Direct  proof,  however,  of  such  damage  is  still  lacking.  Be- 
sides, it  has  been  shown  that  atheroma  is  sometimes  found  in  the  normal 
rabbit  aorta.  In  a  number  of  experiments  by  Gy,  in  which  rabbits 
were  made  to  inhale  smoke  for  a  definite  period  of  time,  only  a  very 
few  were  found  to  have  aortal  changes ;  indeed,  the  proportion  was  not 
more  than  that  usually  in  the  normal  animal.  In  a  study  of  a  large 
series  of  hearts  of  smokers  who  died  from  other  causes,  one  observer 
found  no  changes  except  slight  degeneration  of  the  papillary  muscle 
ascribable  to  the  rapid  heart  action  usual  in  smokers.  Experiments 
have  shown  that  nicotine,  the  main  tobacco  alkaloid,  is  a  powerful 
neurotropic  poison  affecting  particularly  the  sympathetic  ganglia  and 
the  peripheral  vasodilators.  In  view  of  these  observations,  and  in  the  ab- 
sence of  proof  of  pathologic  changes  in  the  human  heart  due  to  tabagism, 
it  is  reasonable  to  assume  that  the  frequent  precordial  pains  and  distress 
are  caused  by  disturbance  in  the  coronary  circulation,  and  by  referred 
pains  from  irritation  of  the  sympathetic  ganglia. 

The  pains  may  be  dull  and  aching,  or  sharp  and  radiating ;  occa- 
sionally, the  first  premonition  is  very  sharp  lancinating  precordial  pain 
radiating  to  the  left  shoulder  and  forearm,  and  accompanied  by  un- 
consciousness. For  example,  a  healthy  man  of  40,  a  heavy  smoker, 
while  running  for  a  train,  was  suddenly  attacked  by  terrific  precordial 
pain'  followed  by  unconsciousness  for  one  hour.  The  cardiovascular 
examination  revealed  nothing  abnormal.  For  weeks  after  the  attack, 
any  slight  movement  —  even  turning  in  bed  —  brought  on  pains. 
The  patient  was  finally  able  to  be  about  and  resume  his  usual  occupation. 
At  present,  six  years  after  the  first  fainting  spell,  he  feels  quite  well. 
He  again  smokes,  but  moderately. 

The  most  frequent  of  the  arrhythmias  in  smokers  are  extrasystole, 
usually  auricular.  Other  arrhythmias,  however,  are  occasionally  en- 
countered. Thus  I  have  seen  two  cases  of  si  no-auricular  block  (Chap- 
ter VII),  one  of  auricular  flutter  and  one  of  auricular  fibrillation. 

Most  cases  of  tobacco  pains  and  arrhythmias  cease  when  smoking  is 
stopped.  Occasionally  both  recur  intermittently  for  years.  In  such 
instances  nitroglycerin  given  regularly,  or  during  pain,  is  of  benefit. 
The  bromides  are  of  value  in  helping  to  control  persistent  arrhythmias. 

B.   Precordial  Pain  of  Extracardiac  Origin 

1.  Gastric  Disturbances.  —  Patients  with  gastric  disturbances,  par- 
ticularly those  in  whom  epigastric  distress  is  marked,  are  apt  to  suffer 


PRECORDIAL  PAINS  269 

from  referred  precordial  pains.  The  clinical  picture  is  that  of  hyper- 
acidity, or  of  gastric  or  duodenal  ulcer.  Belching,  loud  and  explosive 
in  character,  is  usually  a  prominent  symptom.  The  precordial  pains 
are  commonly  sharp,  neuralgic,  fleeting,  and  inconstant  in  character; 
their  distribution  is  usually  along  the  fourth  and  fifth  left  intercostal 
spaces.  Pain  referred  to  the  left  shoulder  is  rare.  Corresponding  to 
the  anterior  distribution,  there  may  be  a  similar  area  posteriorly.  A 
precordial  Head's  zone  is  unusual ;  its  area  of  distribution  inconstant. 
There  may  be  a  close  association  between  gastric  symptoms  and  pre- 
cordial pains,  particularly  when  "  hunger  pains  "  and  belching  are 
marked.  There  is  no  decompensation  or  dyspnoea.  When  gastric 
symptoms  are  stormy,  extrasystoles  may  occur.  Treatment  is  natu- 
rally directed  to  the  underlying  disease.  I  have  found  most  benefit 
from  atropine  given  in  full  physiologic  doses  three  times  a  day  before 
meals,  and  from  an  antacid  powder  containing  equal  parts  of  sodium 
bicarbonate,  magnesium  oxid,  and  oleosaccharated  peppermint  in  half 
teaspoonful  doses  after  meals.  Appropriate  diet  given  frequently  and 
in  small  quantities  is  important.  As  already  noted,  gastric  symptoms 
also  accompany  cardiac  disease,  so  that  the  correlation  and  study  of 
all  the  clinical  data  are  necessary  for  a  correct  diagnosis.  Unless 
extrasystoles  are  subjectively  annoying,  they  require  no  medication ; 
otherwise  they  may  be  partly  controlled  by  bromides. 

2.  Precordial  Pains  from  Esophageal  Disease.  —  Carcinoma,  syph- 
ilis, ulceration,  and  diverticula  are  the  usual  organic  causes  of  referred 
intercostal  and  precordial  pains  of  esophageal  origin.  In  some  cases, 
organic  disease  is  absent ;  the  symptoms  may  then  be  due  to  esophageal 
spasm,  especially  in  the  region  of  the  cardia.  The  usual  symptoms  are 
an  uncomfortable,  conscious  gulping  effort  on  swallowing  solids  or 
fluid,  accompanied  by  sharp  pains  referred  to  the  lower  sternum,  and 
radiating  to  the  precordium  or  even  to  the  upper  and  lower  extremities. 
Such  symptoms  are  occasionally  mistaken  for  those  due  to  aortic  aneu- 
rism ;  and  the  difficulty  in  swallowing,  to  aneurismal  pressure  on  the 
esophagus. 

An  illustrative  case  with  therapy  follows  : 

Male,  aged  48,  stated  that  for  seven  years  he  had  "  choking  sensa- 
tions "  in  the  larynx  and  severe  substernal  pains  on  attempting  to  swal- 
low solid  food.  These  pains  occasionally  radiated  to  the  head,  arms, 
and  legs.  The  symptoms  became  progressively  worse.  The  neurologic 
and  physical  examination  revealed  nothing  abnormal ;  the  fluoroscope 
showed  a  normal  aorta.  Wassermann  reactions  of  the  blood  and  spinal 
fluid  were  negative  ;  the  stools,  urine,  and  gastric  contents  were  normal. 
Roentgenograms  showed  a  pouch-like  dilatation  of  the  middle  part  of 
the  esophagus.  An  esophageal  bougie  was  arrested  opposite  the  middle 
of  the  sternum.  Finally  a  small  bougie  was  passed.  For  purposes  of 
dilatation  bougies  of  increasing  caliber  were  employed.  At  first  semi- 
solid, later  solid  food  was  given.     Atropine  sulphate,  you"  grain  three 


270  CLINICAL   CARDIOLOGY 

times  a  day,  was  administered.  The  pains  gradually  subsided  and 
finally  disappeared.  The  patient  was  taught  to  pass  a  stomach  tube ; 
this  he  did  for  some  weeks  after  he  left  the  hospital.  An  examination 
months  later  showed  that  esophageal  symptoms  and  pains  had  disap- 
peared, and  there  had  been  a  considerable  increase  in  weight. 

3.  Precordial  Pains  Accompanying  Crises  of  Acute  Pulmonary 
Affections.  —  Such  attacks  of  precordial  pain  are  fairly  common  with 
the  crises  of  influenzal  bronchitis,  especially  when  sharp  critical  sweats 
are  present.  Head's  zones  in  the  left  nipple  region,  and  arrhythmias 
(especially  sinus  arrhythmia  and  extrasy stoles),  are  frequent,  a  com- 
bination suggestive  at  first  sight  of  toxic  myocarditis.  Symptoms, 
however,  last  only  a  few  days;  except  for  pain  and  arrhythmia,  the 
heart  is  normal ;  there  is  no  decompensation  or  edema.  Examinations 
made  months  or  years  later  have  shown  that  the  cardiovascular  system 
had  not  been  damaged. 

The  following  is  an  example : 

A  physician,  aged  43,  never  had  any  cardiac  complaint.  He  con- 
tracted pharyngeal  and  bronchial  grippe.  There  were  critical  defer- 
vescence, sharp  sweats,  an  irregular  pulse,  and  sharp  stinging  pains  in 
the  left  breast.  The  patient  feared  that  he  had  an  infectious  myocar- 
ditis, and  carefully  avoided  every  unnecessary  exertion.  Examination 
revealed  a  small  Head's  zone  confined  to  the  left  nipple  region,  and  an 
arrhythmia  which  polygraphic  and  electrocardiographic  tracings  showed 
to  be  due  to  auricular  extrasystoles.  Otherwise  the  cardiovascular 
system  was  normal.  The  patient  was  reassured,  told  to  get  out  of  bed, 
and  given  atropine  sulphate,  y§-^  grain  three  times  a  day  before  meals, 
and  bromides  at  night.  He  was  sent  to  the  country  and  advised  to 
exercise  as  much  as  he  chose.  He  was  soon  able  to  walk  several  miles 
daily.  Within  one  week  the  extrasystoles  and  pain  disappeared,  and 
have  not  since  returned. 

4.  Precordial  Pains  Accompanying  Vasomotor  Disturbances  at  the 
Menopause.  —  Women  at  the  climacteric  period,  with  marked  vaso- 
motor disturbances  (flushes,  heat  flashes,  cold  extremities,  etc.),  fre- 
quently have  persistent  precordial  pains  without  evidence  of  organic 
disease  of  the  heart  or  neighboring  organs.  They  are  possibly  evidence 
of  vasomotor  circulatory  disturbances  in  the  heart  itself.  The  patients 
rarely  react  well  to  medication.  Bromides  and  small  doses  of  atropine 
and  nitroglycerin  are  of  most  value.  Ovarian  (corpus  luteum)  tablets 
are  occasionally  helpful.     Hurry  and  excitement  should  be  avoided. 

5.  Precordial  "  Neuralgias  "  of  Unknown  Origin.  —  Under  this 
heading  is  grouped  a  small  number  of  individuals,  usually  young  and 
apparently  healthy  and  vigorous,  without  vicious  habits,  with  no  rheu- 
matic manifestations,  in  whom  continued  and  frequent  examinations  of 
the  heart  and  other  organs  reveal  nothing  abnormal.  Occasionally, 
sudden  explosive  belching  or  singultus  occurs.  In  one  of  my  cases, 
smoking  some  years  previously  might  have  been  an  etiologic  factor. 


PRECORDIAL  PAINS  271 

The  pains  are  apparently  quite  haphazard  in  their  onset  and  duration, 
and  in  my  experience  defy  medication  and  therapy. 

In  this  group  may  also  be  placed  females  who  complain  of  indefinite 
chest  pains  and  distress,  and  who,  from  other  manifestations,  apparently 
suffer  from  a  functional  disorder  of  an  internal  secretory  organ  or  organs. 
These  patients  are  occasionally  relieved  by  medication  aimed  at  sub- 
stituting the  presumed  secretory  deficiency. 

6.  Pott's  Disease,  Mediastinal  and  Spinal  Tumors,  Tabes,  Inter- 
costal Neuralgia  and  Myalgia,  Pleurisy,  Pericarditis.  —  These  are  ad- 
ditional extracardial  conditions  and  diseases  producing  precordial  pain. 

The  etiology  and  types  of  precordial  pains  here  described  are  ad- 
mittedly incomplete.  Only  those  frequently  encountered  and  clinically 
important  have  been  discussed,  and  their  correlation  with  intra-  or  extra- 
cardiac  disease  described.  It  is  recognized,  also,  that  the  various  groups 
sometimes  overlap.  In  organic  cardiovascular  disease,  I  have  en- 
deavored to  estimate  roughly  the  extent  and  nature  of  the  pathologic 
damage,  and  to  gauge,  if  possible,  the  amount  of  remaining  healthy 
tissue  which  may  be  favorably  influenced  by  therapy.  Thus  studied, 
one  obtains  a  basis  for  rational  therapy,  with  its  prospects  and  limita- 
tions. The  postmortem  specimens  of  advanced  coronary,  endocardial 
and  myocardial  disease,  with  the  history  of  precordial  distress  during 
life,  should  not  blind  us  to  the  fact  that  some  of  these  patients  have 
lived  many  years  despite  their  diseased  organs. 


REFERENCES 
Chapter  XXI 

Adler,  I.,  and  Hensel,  0. :  Intravenous  Injections  of  Nicotine  and  Their  Effects 
upon  the  Aorta  of  Rabbits ;  Journal  of  Medical  Research,  N.S.  X,  229. 

Brooks,  H. :  The  Tobacco  Heart ;  New  York  Medical  Journal,  1915,  CI,  830. 

Curschman,  Angina  Pectoris  —  Discussion  ;  Kongress  fuer  Innere  Medizin,  1891, 
X,  275. 

Foster,  N.  B. :  Uremia ;  Archives  of  Internal  Medicine,  1915,  XV,  536. 

Gy :  L' Intoxication  Tabagique  chez  l'Homme ;  Paris  Theses,  1908-1909, 
203. 

Head  :  Sensibilitaetsstoerungen  der  Haut,  etc.,  1898. 

Huchard :   Diseases  of  the  Heart,  1910,  50. 

Janeway,  T.,  and  Park,  E.  A. :  Question  of  Epinephrin  in  the  Circulation  and 
its  Relation  to  Blood  Pressure ;  Journal  of  Experimental  Medicine,  1912, 
XVI,  541. 

Kent,  A.  F.  S. :  Some  Problems  in  Cardiac  Physiology  ;  British  Medical  Journal, 
July  18,  1914. 

Lewis,  T.,  and  Barcroft,  J. :  Further  Observations  upon  Dyspnoea  and  Its  Re- 
lation to  Blood  Reaction  ;  Quarterly  Journal  of  Medicine,  1914-1915,  VIII, 
97. 

Lucien,  et  Parisot :  Quoted  by  Vaquez ;  Archives  des  Maladies  du  Cceur, 
1915,  VIII,  678. 

Mackenzie,  J. :  Symptoms  and  Their  Interpretations. 

Mackenzie,  J. :   Diseases  of  the  Heart,  2. 


272  CLINICAL  CARDIOLOGY 

Manoue'lian  Y. :  Reeherches  sur  la  Plexus  Cardiaque,  etc. ;  Annales  de  l'lnstitut 

Pasteur,  June,  1914,  579. 
Nothnagel,    H. :    Angina   Peetores   Vasomotoria ;    Deutsches   Archiv  f .    klin. 

Medizin,  1867,  V,  3,  209. 
Oppenheimer,  B.  S.,  and  Oppenheimer,  A. :   Nerve  Fibrils  in  the  Sino-auricular 

Node ;  Journal  of  Experimental  Medicine,  1912,  XVI,  613. 
Osier  and  McCrae  :   System  of  Medicine,  IV,  449. 
Sherrington  :   Integrative  Action  of  the  Nervous  System. 
Stein,  R. :  Angina  Pectoris ;  Medical  Record,  1915,  LXXXVIII,  131. 
Wilson,  J.  6.   :    The  Nerves  of  the  Atrio-ventricular  Bundle ;   Proceedings  of 

the  Royal  Society,  1909,  LXXXI,  Series  B. 


CHAPTER  XXII 

THERAPY    OF    PNEUMONIA    FROM    THE    CIRCULATORY 

STANDPOINT 

Because  of  the  frequency  with  which  cardiac  drugs  are  employed 
in  pneumonia,  I  wish  to  review  my  impressions  gained  in  the  drug  treat- 
ment of  many  cases  of  pneumonia.  I  shall  not  touch  upon  the  bac- 
teriological or  chemotherapeutical  aspects.  Statistical  study  of 
various  epidemics  or  methods  of  treatment  have  likewise  not  been 
dwelt  upon.  Indeed,  it  is  because  I  feel  that  none  of  the  methods 
of  medicinal  treatment  has  been  followed  by  any  demonstrable  corre- 
lation of  cause  and  effect,  or  of  therapy  and  subsequent  cure,  that  I 
have  discarded  statistics  as  bringing  us  no  nearer  to  the  therapeutic 
and  circulatory  problems  of  pneumonia.  A  study  of  these  methods, 
some  of  them  directly  antagonistic  in  theory  and  practice,  arouses  doubt 
as  to  their  possible  efficacy.  Mere  mention  of  some  of  the  types  of 
treatment,  many  long  since  discarded,  may  therefore  not  be  amiss. 
Creosote,  alcohol,  no  treatment  until  the  crisis,  no  treatment  for  hyper- 
pyrexia, cold  sponges  or  even  tubs  for  the  same  symptom,  no  stimulation, 
stimulation  at  the  crisis  only,  stimulation  to  prevent  the  dangers  of  the 
crisis,  camphor  in  oil,  caffein,  digitalis,  adrenalin,  venesection,  fresh 
air,  cold  air,  are  or  have  been  popular. 

"  Stimulation  "  has  been  the  usual  therapeutic  keynote,  for  the 
danger  was  always  correctly  conceived  to  be  circulatory  failure.  I  have 
used  all  of  the  recognized  cardiotonics  —  digitalis,  strophanthus,  caffein, 
adrenalin,  as  well  as  those  whose  effect  upon  the  circulation  may  well  be 
questioned  —  alcohol,  strychnine,  camphor.  Camphor  I  have  used  in 
smaller,  repeated,  as  well  as  in  several  larger  hypodermic  injections, 
though  experiments  have  shown  that  camphor  in  oil  had  no  effect  in 
delaying  or  preventing  death  in  artificially  induced  pneumonia.  I 
have  employed  the  other  drugs  mentioned  in  all  possible  forms  and 
combinations ;  in  heroic,  in  small  and  moderate  doses,  subcutaneously, 
intravenously,  and  internally,  before,  during,  and  after  the  crisis.  With 
possible  isolated  exceptions,  I  have  yet  to  see  any  of  the  effects  upon 
the  circulation  which  follows  the  use  of  some  of  these  drugs  in  the  ex- 
perimental animal,  or  in  cardiac  failure  from  cardiovascular  disease. 

T  273 


274  CLINICAL  CARDIOLOGY 

The  chief  reasons  for  disappointment  in  pneumonia  therapy  are,  I 
believe,  that  we  are  dealing  with  an  infection  of  varying  virulence  and 
involving  varying  amounts  of  lung  tissue.  Therefore  I  have  attempted, 
for  clinical  and  therapeutic  purposes,  to  roughly  group  and  to  treat 
pneumonia  according  to  degrees  of  toxicity  and  the  extent  of  lung 
involvement.     I  consider  the  crisis  a  separate  problem  for  therapy. 

1.  Toxic  Cases.  —  In  the  extremely  toxic  group,  typically  exempli- 
fied by  sharp  onset,  early  delirium,  subsultus,  dry  tongue,  no  pain, 
rapid  pulse  and  breathing,  my  experience  has  been  that  attempts  at 
"stimulation,"  a  term  which  we  shall  apply  to  drug  therapy  used  to 
combat  and  treat  circulatory  failure,  are  almost  always  without  efficacy. 
These  patients  apparently  defy  all  drug  therapy  and  sometimes  die 
before  the  area  of  pneumonic  involvement  becomes  clinically  recognizable. 
Death  ensues  from  acute  toxemia.  Stimulation,  even  if  heroic,  has  not 
in  my  hands  in  any  visible  manner  delayed  or  prevented  the  fatal  out- 
come. The  reason  is  apparently  because  the  drugs  do  not  combat  the 
infective  factor.  Experiments  throw  an  interesting  sidelight  upon  this 
problem.  It  has  been  found  that  hearts  perfused  with  pneumonic  blood 
lose  their  efficiency,  which  is  later  restored  by  the  use  of  normal  blood. 
Whether  in  the  human  being  the  changes  wrought  in  the  cardiac  muscu- 
lature are,  or  later  become,  myocarditis  are  questions  into  which  we  shall 
not  enter. 

It  is  usually  believed  that  in  toxic  pneumonia  there  is  marked  vaso- 
motor failure,  though  others,  as  the  result  of  animal  experimentation, 
have  held  otherwise.  I  have  only  very  rarely  seen  any  therapeutic  re- 
sult from  single  or  repeated  injections  of  adrenalin  given  subcutaneously 
or  intravenously.  A  like  negative  result  has  almost  regularly  followed 
the  use  of  strophanthin  and  other  digitalis  bodies  when  the  pulse  was 
regular.  That  digitalis  does  localize  itself  and  affect  the  heart  muscle 
in  pneumonia  as  in  purely  cardiac  disease  has  recently  been  shown  by 
A.  E.  Cohn,  who  found  the  usual  electrocardiographic  evidence  of  digi- 
talization  —  a  negative  T  wave  (Chapter  VI).  Despite  this  change  in 
the  electrocardiogram,  I  have  found,  in  rhythmic  cases,  no  evidence  of 
any  help  to  the  circulation  from  digitalis  —  cyanosis  was  not  de- 
creased, dangers  from  edema  of  the  lungs  not  reduced. 

As  a  favorable  prognostic  sign,  Gibson  has  emphasized  a  certain 
parallelism  between  pulse  rate  and  systolic  blood  pressure ;  but 
others  as  well  as  myself  have  found  his  so-called  law  of  no  significance. 
The  removal  of  500  to  700  c.c.  of  blood  by  venesection  gives  occasional 
temporary  relief  in  toxic  cases ;  the  benefit  seems  attributable  to  ridding 
the  body  of  toxic  material  rather  than  from  any  primary  circulatory 
relief. 

2.  Area  of  Pneumonic  Involvement.  —  With  no  evidence  of  severe 
toxemia,  slowly  progressing  consolidation  confined  to  one  lung  is  usually 
not  dangerous  during  the  acute  febrile  period.  Such  are  probably  the 
cases  in  which  no  treatment  or  any  treatment  has  its  measure  of  success. 


THERAPY  OF  PNEUMONIA  275 

If,  however,  there  is  massive  sudden  involvement  of  one  entire  lobe  and 
part  or  all  of  another,  the  inflamed  area  in  itself  offers  a  problem  for 
therapeusis,  aside  from  the  question  of  toxicity  and  crisis;  for  the 
pulmonary  circulation  may  be  sufficiently  interfered  with  to. produce 
cyanosis  and  beginning  circulatory  failure.  Here  venesection  is  clearly 
indicated  for  the  relief  of  pulmonary  stasis  ;  "  stimulation  "  has  a  better 
chance  for  success,  for  the  problem  approaches  more  nearly  a  purely 
circulatory  one.  Cardiac  tonics  should  be  given  in  large  doses  from  the 
very  outset,  to  combat,  if  possible,  ever  impending  circulatory  failure. 

3.  The  crisis  apparently  marks  that  point  at  which  there  is  more 
or  less  complete  sudden  destruction  of  the  pneumococci  in  the  lung, 
while  lysis  marks  their  more  gradual  destruction.  The  main  dangers 
during  crisis  are  general,  from  sudden  systemic  toxic  invasion ;  and 
local,  from  edema  of  the  lungs.  The  local  danger,  from  the  circulatory 
standpoint,  depends  upon  the  amount  and  rapidity  of  resolution,  and 
consequent  pulmonary  edema.  An  extremely  important  factor,  scarcely 
mentioned  in  the  literature,  is  the  presence  or  absence  of  expectoration 
at  the  crisis.  Pulmonary  edema  complicates  and  accompanies  resolu- 
tion more  frequently  if  expectoration  is  absent ;  while  if  expectoration 
takes  place,  there  is  increasing  opportunity  for  pulmonary  aeration, 
and  less  for  edema.  I  always  insistently  try  to  make  the  patients 
cough  in  the  hope  of  loosening  and  expectorating  the  pneumonic  prod- 
ucts. When,  despite  this,  edema  of  the  lungs  supervenes,  as  shown  by 
the  loud  mucous  bubbling  rales  over  the  pneumonic  and  other  areas  of 
the  chest,  the  chances  for  success  become  less,  but  even  then  I  have  the 
attendant  regularly  rouse  the  patient  to  coughing  efforts  as  long  as 
consciousness  is  retained.  As  far  as  one  may  judge,  stimulation  in 
acute  pulmonary  edema  occasionally  keeps  the  patient  alive  for  some 
hours  or  even  a  day,  and  may  exceedingly  rarely  seem  to  pull  a  patient 
from  death. 

With  lytic  or  gradual  resolution,  even  with  very  sharp  critical 
drops  of  temperature,  the  battle  is  usually  won,  for  edema  of  the  lungs 
rarely  occurs  and  stimulation  may  be  efficacious.  However,  even  in 
cases  of  non-massive  pneumonic  involvement  in  young,  vigorous  indi- 
viduals, with  no  evidence  of  toxicity  during  the  attack,  sudden,  almost 
tragic  intrusion  of  critical  resolution,  edema  of  the  lungs,  and  death  — 
all  within  a  few  hours  —  may  supervene.  One  instance  especially  im- 
pressed me  —  that  of  a  young,  healthy  individual  to  whom  the  pneu- 
monia was  literally  a  laughing  matter.  From  the  presence  of  perspira- 
tion and  from  the  physical  signs  in  the  lungs,  I  was  able  to  foretell  the 
onset  of  critical  resolution  some  hours  before  the  typical  drop  in  tem- 
perature. Heart  and  pulse  were  then  perfectly  satisfactory.  Her- 
culean efforts  were  made  by  stimulation  and  otherwise  to  ward  off  the 
dangers  of  edema  of  the  lungs.  Within  six  hours,  however,  the  patient 
died  from  pulmonary  edema  ;  while  in  an  adjoining  ward,  an  old  woman, 
severely  poisoned  by  her  pneumonia  and  very  sick  for  over  one  week, 


276  CLINICAL   CARDIOLOGY 

had  reached  the  crisis  with  slow,  gradual  resolution  of  the  pneumonia, 
and  was  slowly  and  surely  convalescing. 

Where  digitalis  has  been  given,  its  effect  in  causing  arrhythmia 
must  naturally  be  considered.  Aside  from  this,  a  study  of  cardiac 
irregularities  occurring  during  the  course  of,  and  at  the  crisis  of,  pneu- 
monia offers  interesting  and  important  therapeutic  problems.  The 
usual  types  are  moderate  bradycardia,  sinus  arrhythmia,  extrasy stoles, 
auricular  fibrillation,  and  heart  block.  It  is  sometimes  assumed  that 
the  presence  of  the  arrhythmias  is  indicative  of  some  organic  affection  of 
the  cardiac  valves,  or  of  the  musculature.  But,  as  in  the  non-pneumonic 
individual,  irregular  heart  action  does  not  in  itself  necessarily  mean  heart 
disease.  Indeed,  some  of  these  arrhythmias  —  especially  sinus  arrhyth- 
mia, moderate  bradycardia,  and  extrasystoles  —  when  found  with  an 
unembarrassed  circulation,  at  or  immediately  after,  the  crisis  usually 
offer  good  clinical  evidence  that  the  disease  has  definitely  run  its  course. 
The  irregular  cardiac  action  is  apparently  due  to  a  neurotropic  effect 
of  pneumonic  toxins.  Whether  the  latter  act  upon  the  medullary 
center  or  upon  the  heart  itself  it  is  impossible  to  state.  Because  of 
their  occurrence  at  the  time  of  crisis,  and  because  some  drugs  (for  ex- 
ample, morphine)  produce  arrhythmias  by  affecting  the  cardio-inhibitory 
center,  I  am  inclined  to  the  former  view.  These  arrhythmias  usually  last 
a  few  hours  or  days.  I  have  followed  some  of  these  cases  for  years  and 
have  never  observed  any  correlation  between  the  arrhythmias  and  the 
possible  later  development  of  organic  cardiovascular  disease. 

I  have  observed  auricular  fibrillation  —  complete  irregularity  of  the 
pulse  —  several  times  at  the  crisis.  In  three  such  patients,  each  of 
whom  had  several  crises  from  successive  involvement  and  resolution  of 
various  pulmonary  areas,  there  were  attacks  of  fibrillation  lasting  several 
hours  with  each  crisis.  Two  of  the  patients  were  elderly ;  the  third,  a 
vigorous  adult.  None  showed  circulatory  embarrassment  or  heart 
failure  during  the  course  of  the  fibrillation ;  on  the  contrary,  there  was 
the  usual  picture  seen  in  favorable  crises  with  normal  rhythm.  On  the 
other  hand,  I  have  observed  other  cases  of  auricular  fibrillation  occurring 
during  the  course  of  toxic  pneumonia,  all  of  whom  died.  In  these  it 
was  impossible  to  estimate  how  much  the  arrhythmia  itself  contributed 
to  the  dangers  of  the  pneumonia. 

Complete  heart  block  with  slow  ventricular  rhythm  is  rarely  found 
in  pneumonia.  That  it  may  be  functional  in  origin  and  probably  due 
to  abnormal  action  upon  the  cardio-inhibitory  center  seems  indicated 
by  two  of  my  cases,  one  of  which  came  to  necropsy.  The  patient  had 
been  ill  for  some  time,  there  was  no  history  of  digitalis  medication. 
Microscopically  and  grossly,  the  cardiac  musculature  and  the  bundle 
of  His  were  found  normal. 

The  therapeusis  of  arrhythmias  developing  in  pneumonia  is  similar 
to  that  in  non-pneumonic  individuals.  If  accompanied  by  heart  failure, 
the  arrhythmias  are  of  serious,  possibly  ominous  import.     Except  in 


THERAPY   OF   PNEUMONIA  277 

heart  block  with  slow  ventricular  activity,  when  atropine  should  be  tried, 
the  treatment  of  these  arrhythmias  is  no  different  from  that  of  the  other 
phases  of  pneumonia  already  discussed.  If  arrhythmias  are  unaccom- 
panied by  failing  circulation,  though  they  perhaps  should  not  be  entirely 
disregarded,  their  import  is  slight  and  they  rarely  require  separate 
medication. 


REFERENCES 
Chapter  XXII 

Cohn,  A.  E. :  Clinical  and  Electrocardiographic  Studies  on  the  Action  of  Digi- 
talis ;   Journal  of  the  American  Medical  Association,  1915,  LXV,  1527. 

Hektoen,  L.  :  The  Mechanism  of  Recovery  in  Pneumonia  ;  Journal  of  the 
American  Medical  Association,  1914,  LXII,  254. 

Hirschfelder,  A.  D.,  and  Winternitz,  M.  C.  :  Studies  upon  Experimental  Pneu- 
monia in  Rabbits  ;  Journal  of  Experimental  Medicine.  1913,  XVII,  667. 

Neuhof ,  S. :  Functional  Heart  Block  in  Pneumonia ;  Journal  of  the  American 
Medical  Association,  1914.  LXIII.  577. 

Newburgh,  L.  H.  :  The  Use  of  Strychnine  and  Caffein  as  Cardio-vascular 
Stimulants  in  the  Acute  Infectious  Diseases  ;  Archives  of  Internal  Medicine, 
1915,  XV,  458. 

Newburgh,  L.  H.,  and  Porter,  W.  T. :  The  Heart  Muscle  in  Pneumonia  ;  Journal 
of  Experimental  Medicine,  1915,  XXII,  123. 

Porter,  W.  T.,  and  Newburgh,  I. :  Vasomotor  Apparatus  in  Pneumonia  ;  Amer- 
ican Journal  of  Physiology,  1914,  XXV,  1. 


INDEX 


a   Wave 

auricular  fibrillation  and,  82 

bifurcated,  16 

in  complete  heart  block,  90 

in  nodal  extrasystole,  69 

in  sinus  arrhythmia,  82 

in  true  bradycardia,  79 

normal,  14,  15 

prominent,  17 

visible  in  jugular  pulsations,  129 
a-c-v  Waves 

description  of,  14-15 
Acidosis 

definition  of,  168 

dyspnoea  from,  168-169 

heart  block  from,  102 

in  diabetes,  151 

in  nephritis,  233 

in  uremia,  247 

with  hypertension,  260-261 
Aconite 

effect  on  heart  rate,  220 

extrasystoles  from,  220 
Adhesions 

causing  cardiac  displacement,  30 
Adrenalin 

iSee  Suprarenal  Extract 
Alcohol 

clinical   symptoms  of  alcoholism, 
150 

effect  on  blood  pressure,  246 

effect  on  circulation,  220 

endocarditis  from,  150 

fatty  degeneration  of  myocardium  from 
163 

myocarditis  from,  150 

use  in  pneumonia,  276 
Amtl  Nitrite,  219 
Anaphtlotoxins 

in  heart  block,  102 
Anasarca 

in  chronic  endocarditis,   169 

Karrell  diet  in,  218 
Anemia 

cerebral  —  see  Cerebral  Anemia 

dyspnoea  in,  168-169 

functional  murmurs  in,  143-145 

in  rheumatic  endocarditis,  167-175 

in  streptococcus  viridans,  179-180 

in  uremia,  262 

myocarditis  from,  160,  162,  163 


Angina  Pectoris 

See  Precordial  Pains 
Aorta 

elasticity  of,  19 

enlargement  of,  122 

in  aortic  lesions,  118,  119,  121,  122 

in  cardiosclerosis,  164,  195 

in  fetal  heart,  2 

in  hypertension,  261 

in  orthodiascopic  tracing,  111 

in  syphilis,  158 

lead  poisoning  and,  149 

origin  of,  1 

palpation  of,  133 

percussion  of,  135-136 

physical  examination  of,  137 

pulsations  of,  130,  186 

standards  of  measuring,  121 
Aorta,  Aneurismal  Dilatation  of 

aortic  pulsation  in,  186 

definition  of,  185,  186 

diagnosis  of,  121,  122,  190 

differential  diagnosis,  191 

etiology      of       substernal      pains       in, 
189 

heart  sounds  in,  185,  190 

in  aortitis,  195-196 

in  cardiosclerosis,  194 

in  tertiary  cardiac  syphilis,  184 

murmurs  in,  185-186,  190 

orthodiascopy  in,  121,  185,  191 

palpation  in,  133 

pathology  of,  185 

percussion  in,  135 

prognosis  in,  192-193 

roentgenogram    of,    191 

site  of,  185,  193 

symptomatology  of,  189-192,  193 

therapy  of,  189,  192,  213 
Aortic  Aneurism,  Sacculated 

precordial  pains  in,  267 

symptoms  of,  267 

therapy  of,  267 
Aortic  Arch 

in  cardiosclerosis,  195 

in  myocardial  insufficiency,  263 

orthodiascopic  tracing  of,  111-112 

physical  examination  of,  137 
Aortic  Bulb 

division  of,  1 

origin  of,  1 
279 


280 


INDEX 


Aortic  Pulsation 

cause  of  severe,  130 

clinical  recognition  of,  130 

clinical  significance  of,  130 

in  aneurisms,  130 

in  aneurismal  dilatations,  130 

in  cardiosclerosis,  195 

inspection  in,  130 

palpation  in,  133 
Aortic  Regurgitation 

aortic  pulsation  in,  130 

chest  palpation  in,  133 

hemoptyses  in,  173 

length  of  life  with,  176 

low  dicrotic  notch  in,  20 

murmurs  in,  141 

reduplicated  apical  impulse  in,  147 

symptoms  of,  173 

systolic  blood  pressure  in,  248 
Aortic  Stenosis 

and  pulsus  bisferiens,  20 

chest  palpation  in,  132,  133 

congenital,  122,  124 

murmurs  in,  141,  142,  143,  145 

orthodiascopy  in,  120 

polygram  of,  17 

pulsus  tardus  in,  141 

symptoms  of,  172 

therapy  of,  123 
Aortic  Valves 

bacterial  invasion  of,  158 

cause    of   reduplicated    second    sound, 
146 

in  cardiac  syphilis,  184 

in  extrasystole,  54 

physical  examination  of,  137 

position  of,  2 

relation  to  dicrotic  wave,  19 
Aortic  Valvular  Lesions 

carotid  pulse  in,  130 

combined    with    mitral    lesions,     120, 
248 

digitalis  in,  214 

fluoroscopy  in,  118,  119 

pregnancy  of  women  with,  239-240 

regurgitant,  130 
Aortitis 

aorta  in,  121 

carotid  pulse  in,  130 

causes  of,  121 

heart  sounds  in,  150 

in  alcoholism,  150 

in  cardiac  syphilis,  184 

in  cardiosclerosis,  194-195 

in  diabetes,  151 

in  lead  poisoning,  149 

in  tabagism,  150-151 

luetic,  133 

orthodiascopy  in,  120-122 

reduplicated   apical  impulse  in,    146 

with  left  ventricular  hypertrophy,   33 
Aphasia 

in  decompensated  mitral  stenosis,   172 


Apical  Region 

clinical  significance  of,  130 

factors  influencing  inspection  of,  131 

in  abnormal  ventricular  action,  131 

in  auricular  fibrillation,  131 

in  heart  block,  131 

in  mitral  stenosis,  130 

in  premature  contraction,  131 

in  respiratory  phases,  131 

inspection  of,  130-131 

position  of,  137,  138 
Apocynum,  216 
Appendicitis 

bradycardia  in,  100 
Arrhythmias 

causes  of,  47 

classification,  47,  48 

digitalis  in,  206-209,  215 

diagnosis  of,  48 

etiology  of,  96-109 

from  tabagism,  151,  268 

in  acute  rheumatic  endocarditis,  167 

in  pneumonia,  276-277 

in  streptococcus  viridans,  181 

therapy  of,  100,  206-209,  215-217 
Arsenic 

action  of,  150 

myocarditis  from,  163 
Arterial  Tracing 

blending  of  venous  with,  16 

normal,  14,  15,  16 
Arterial  Wall 

relation  to  blood  pressure,  243 
Arteriogram 

See  Arterial  Tracing 
Arteriosclerosis 

from  syphilis,  159 

in  diabetes,  151 

murmurs  differentiated  from  valvular 
lesions,  142,  143 

murmurs  in,  142-143 
Arteriosclerosis,  Premature 

blood  pressure  in,  248,  267 

course  of,  266    . 

etiology  of,  267 

precordial  pains  in,  266-267 

symptoms  of,  266 

treatment  of,  267 
Arteriosclerosis,  Senile 

blood  pressure  in,  248 

causing  aortitis,  121 

precordial  pains  in,  267 

symptoms  of,  267 

therapy  of,  267 
Asphyxia 

in  animals,  causing  heart  block,   101- 
102 
Asthenic  Heart 

See  "Weak"  Heart 
Atrio-ventricular  Node 

disturbance  in,  48 

excitation  wave  in,  44 

in  arrhythmias,  79 


INDEX 


281 


Atrioventricular  Node   (Continued) 

nodal  extrasystoles,  69,  74 

rate  of,  in  complete  heart  block,  85 

seat  of  rhythmic  impulse  formation,  49 
Atropine 

combined  with  digitalis,  209-210,  215 

effect  on  heart,  45,  106 

in  bradycardia,  100 

in  digitalis  arrhythmias,  206-207 

in  heart  block,  90,  101,  103 

in  myocardial  insufficiency,  263 

in  pneumonia,  277 

in  precordial  pains,  261,  269,  270,  289 

in  sino-auricular  block,  97 

in  ventricular  escape,  108,  109 

in  "weak"  heart,  257 
Auricle 

abnormal    sequence    of    contraction    of 
auricles,  48 

asynchronous    contraction   of   auricles, 
34,  36,  47 

ectopic  contraction  of,  51 

excitation  wave  in,  44 

in  orthodiascope  tracing,  111 

musculature  of,  3 

origin  and  development  of,  1 

premature  contraction  of,  48,  52 
Auricular  Asynchronism 

electrocardiogram  of,  34,  35,  36 
Auricular  Beat,  Blocked 

classified,  48 

description  of,  83 

differentiation  from  extrasystoles,  83 

differentiation       from       sino-auricular 
block,  83 
Auricular  Contraction 

as  cause  of  reduplicated  first  sound,  146 

asynchronous,  34,  36,  47 

electrocardiographic  complex  of,  25 

incoordinate,  47,  56,  67—68 
Auricular  Dl\stole 

effect  on  a-c-v  waves 
Auricular  Fibrillation 

absence  of  a  wave  in,  14,  58 

as  cause  of  decompensation  in  mitral 
stenosis,  172 

auricular  activity  in,  56 

cardiac  palpation  in,  134 

caused  by  tabagism,  105,  268 

classification  of,  47,  68 

clinical  recognition  of,  58,  60,  62,  64 

differentiation    from    coupled    rhythm, 
54 

differentiation  from  extrasystole,  54,  64 

differentiation  from  paroxysmal  tachy- 
cardia, 62 

differentiation  from  simple  tachycardia, 
55 

differentiation  from   sinus  arrhvthmia, 
82 

digitalis  in,  206,  207,  210-211,  214,  237 

diseases  accompanied  by,  104,  105 

etiology  of,  104,  105 


Auricular  Fibrillation  (Continued) 
in  acute  endocarditis,  166 
in  aortic  regurgitation,  173 
in  aortic  stenosis,  172 
in  cardiosclerosis,  198,  199,  202 
in  decompensated  mitral  regurgitation, 

170 
in  diphtheria,  152 
in  normal  hearts,  105 
in  pneumonia,  276 
inspection  of  apical  region  in,  131 
jugular  pulsations  in,  130 
liver  pulsation  in,  132 
marriage  of  women  with,  237-239 
method   of   estimating   blood   pressure 

in,  250-251 
murmurs  in,  140 
occurrence  of,  104,  105 
orthodiagram    of,    with   mitral   lesions, 

117 
pathology  of,  56,  58 
pregnancy  of  women  with,  239 
strophanthin  in,  215 
therapy  of,  105,  207,  211,  214 
transient,  63 

ventricular  activity  in,  56 
with  auricular  flutter,  63,  66,  68 
with  coupled  rhythm,  64 
with  mitral  stenosis,  56,    58,    60,    104, 

176,  214 
Auricular  Flutter 
classification,  47,  68 
clinical  recognition  of,  68 
differentiation  from  fibrillation,  67,  68 
differentiation  from  heart  block,  67 
digitalis  in,  207 
electrocardiographic  recognition  of,  66, 

67 
etiology  of,  56,  107 
from  tabagism,  268 
in  acute  endocarditis,  166 
jugular  pulsations  in,  130 
occurrence,  107 

polygraphic  recognition  of,  64,  65 
therapy  of,  107,  207 
Auricular  Systole 

cause  of  a  wave,  14-15 
in  auricular  flutter,  67 
jugular  pulse  in,  129 
Auricular  Tachtsvstole 
See  Auricular  Flutter 

AURICULO-VENTRICULAR     CONDUCTION    SYS- 
TEM 

arterial  supply  of,  9,  10 

comparison   with    sino-auricular   node, 

10 
dissection  of,  9 
distribution  of,  8,  9 
excitation  wave  in,  44,  45 
in  auricular  fibrillation,  56 
in  bundle-branch  lesions,  77 
in  heart  block,  101 
moderator  band  of,  9 


282 


INDEX 


AURICULO-VENTRICULAR    CONDUCTION    SYS- 
TEM (Continued) 
nerve  supply  of,  9,  10 
position  of,  8,  9 
Purkinje  fibers,  9 

relation  of  sino-auricular  node  to,  7,  8 
seat  of  rhythmic  impulse  formation,  49 
structure  of,  9 
terminal  aborizations  of,  9 

AURICULO-VENTRICULAR    VALVES 

effect  on  a-c-v  waves,  16 
effect  on  first  heart  sound,  147 
effect  on  third  heart  sound,  145 
Auscultation  of  Heart 

in  aneurismal  dilatation  of  aorta,  185— 

186,  190 
in  aortic  regurgitation,  141 
in  aortic  stenosis,  141 
in  aortitis,  195-197 
in  auricular  fibrillation,  140 
in  cardiosclerosis,  195 
in  combination  of  lesions,  142 
in  mitral  regurgitation,  139 
in  mitral  stenosis,  139-141 
in  myocarditis,  195-197 
in  pulmonary  stenosis,  142 
in  tricuspid  valvular  lesions,  141,  142 
in    valvular    pulmonary    insufficiency, 

142 
influencing  factors  in,  139 
reduplicated  second  sounds  in,  146 
supplemented    by    other    methods    of 

examination,  137 
value  of,  129,  138 

Backward  Conduction,  84 
Baths 

See  Hydrotherapy,  and  Baths,  Car- 
bon Dioxide 
Baths,  Carbon  Dioxide 

action  of,  225,  253 

at  Nauheim,  226 

effect  on  blood  pressure,  225-226,    253, 
261 

method  of  producing,  at  home,  226 

types  of  patients  suitable  for,  226 
Baths,  Electric  Light 

for  hypertension,  261 
Belching 

in   precordial   pains   of   gastric   origin, 
269 
Beverages 

in   compensated   valvular   disease,  229 

in  uremia,  263 
Blood 

carbon  dioxide  tension  of,  168 

chemical  examination  of,  233-234,  247, 
260-261 

creatinine  in,  233 

in  cyanosis,  168-169 

in  hypertension,  260-261 

in  streptococcus  viridans,  179-180 

in  tertiary  cardiac  syphilis,  184 


Blood  (Continued) 

in  uremia,  247,  263 
non-protein  nitrogen  in,  233-234,  260 
relation  to  blood  pressure,  242,  243 
viscosity  of,  243 
volume  of,  243 
Blood  Cultures 

in  streptococcus  viridans,  181 
Blood  Pressure 

after  meals,  245-246 

alcohol  and,  220,  246 

carbon  dioxide  baths  and,  225-226 

cardiac  energy  and,  242 

clinical  estimation  of,  243-246 

cyanosis  and,  213,  246 

digitalis  and,  192,  213,  246 

diurnal  variations  of,  245 

elasticity  of  arterial  wall  in,  243 

excitement  and,  246 

exercise  and,  246 

in  aortic  regurgitation,  248 

in  cardiac  arrhythmias,  250-251 

in  cyanosis,  249 

in  edema,  244 

in  exophthalmic  goiter,  248 

in  functional  efficiency  tests,  236-237 

in  hyperpiesis,  249 

in  hypertensive  cardiovascular  disease 

with  myocarditis,  246-247 
in     hypertensive     myocardial     insuffi- 
ciency, 246,  262 
in  hypotension,  249-250 
in  increased  intracranial   tension,   249 
in  lead  poisoning,  248-249 
in  mitral  lesions,  248 
in  myocardial  disease  and  insufficiency 

without  hypertension,   248,   260-263 
in  organic  cardiovascular  disease,  246- 

248 
in  senile  and  premature  arteriosclerosis, 

248,  266,  267 
in  uremia,  246,  262 
in  valvular     disease     and     myocardial 

insufficiency,  248 
influence  of  respiration  on,  245 
methods  of  determining  systolic,    243- 

245 
necessity   of    frequent    estimations  of, 

246 
nitroglycerine  and,  219 
normal  diastolic,  245 
normal  systolic,  245 
peripheral  resistance  and,  242-243 
physiological  considerations,  242 
smoking  and,  246 
sparteine  and,  220 
sphygmomanometer,  243-245 
strychnine  and,  219 
systolic  output  in,  236-237 
therapy  of,  251-253,  261-262 
venesection  in,  246 
viscosity  of  blood  and,  243 
volume  of  circulating  blood  and,  243 


INDEX 


283 


Brachial  Artery 

in  estimation  of  blood  pressure,  243- 
245 
Bradycardia,  Spurious,  78 
Bradycardia,  True 

classification,  47 

clinical  recognition  of,  79 

definition  of,  78 

differentiation  from  heart  block,  79 

electrocardiogram  of,  78 

etiology  of,  99,  100 

in  cerebral  anemia,  249 

in  pneumonia,  276 

occurrence,  99,  100 

rate  in,  78,  79 

symptoms  of,  78 

therapy  of,  100 
Broad  Heart 

description  of,  114,  115 

orthodiagram  of,  113,  114 
Bromides 

in   acute   rheumatic  endocarditis,   174, 
264 

in  auricular  fibrillation,  105 

in  extrasy stoles,  97,  99,  221,  269 

in  paroxysmal  tachycardia,  106 

in  precordial  pains  at  menopause,  270 

in  simple  tachycardia,  106,  221,  237 

in  tabagism,  268 
Bronchitis 

as  indicating  bronchial  congestion,  169 

as  symptom  of  decompensated  mitral 
regurgitation,  170 

extrasystoles  in,  98 

in  endocarditis,  169 

in  pregnant  women  with  cardiac  lesions, 
239 

precordial  pains  in  crisis  of,  270 

sinus  arrhythmia  in,  96 
Bruit  de  Rappel,   145 
Bundle-branch  Lesions 

classification,  47 

description  of,  77 

differentiation  of  electrocardiogram  of 
cardiac  hypertrophy  from,  77 

electrocardiogram  of,  77 

reduplicated  apical  impulse  in,  146-147 

types  of,  77 
Bundle  of  His 

see  auriculo-ventricular    conduc- 
TION System 

c   Wave  (see  also  a-c-v  Waves) 

in  complete  heart  block,  90 

in  nodal  extrasystole,  69 

in  true  bradycardia,  79 

split,  16 
Caffein 

derivatives  of,  216-219 

dose  of,  216 

effect  on  heart,  216 

effect  on  kidneys,  216 

extrasystoles  from,  99 


Caffein  (Continued) 

in  pneumonia,  273 

tachycardia  from,  106 
Calisthenics 

cardiac  disease  and,  224,  236 

"weak"  heart  and,  257 
Calomel 

dosage,  221-222 

use  of,  221-222 
Camphor 

effect  of,  220 

in  pneumonia,  273 
Canadian  Hemp 

See  Apocynum 
Cardiac  Displacements 

causes  of,  30 

classification,  28 
Cardiac  Efficiency 

See  Functional  Efficiency  Tests 
Cardiac  Energy 

mechanism  of,  242 

relation  to  blood  pressure,  242 
Cardiac  Failure 

See   Decompensation,     and    Myocar- 
dial Insufficiency 
Cardiac  Malformations,  Congenital 

orthodiascopy  of,  122-128 
Cardiac  Neurosis 

carbon  dioxide  baths  for,  226 

hydrotherapy  for,  224-225 
Cardiac     Outline     {see   also    Orthodia- 
scope Tracing) 

mapped  out  by  percussion,  135,  137 

methods    for    determining,    135,    137- 
138 

relation  to  physique,  137-138 
Cardiac  Paralysis 

in  diphtheria,  152 
Cardiac  Rate 

action    of   digitalis   on,    213    (see   also 
Digitalis) 

importance  of  radial  tracing,  18 
Cardiac  Syphilis 

aneurismal  dilatations  in,  184,  185-193 

aneurisms  in,  184 

clinical  symptoms  of  tertiary,  184-185 

diagnosis  of,  184 

effect  on  heart  valves,  184 

heart  block  in,  101 

myocardial  involvement  in,  184 

pathology  of,  158,  159 

precordial  pains  in,  266 

therapy  of,  266 

valvular  disease  and,  158,  159 
Cardiac  Tube 

crista  terminalis  of  His,  1 

development  of,  1 
Cardio-inhibitory  Center 

relation  to  extrasystoles,  97,  98,  99 

relation  to  heart  block,  101,  102 

relation  to  sinus  arrhythmia,  96 
Cardio-nephritis 

ventricular  arrhythmia  in,  68 


284 


INDEX 


Cardio-renal  Disease 

effect  of  theobromine  sodium  salicylate 

on,  217 
Karrell  diet  in,  218-219 
pathology  of,  164 
Cardiosclerosis 

(See  also  Myocarditis) 
aortic  dilatation  in,  186,  194-195 
arrhythmias  in,  198,  202 
auricular  fibrillation  in,  62-63,  198 
cardiac  syphilis  and,  184 
caused  by  pneumonia,  154-155 
complications  of,  199 
digitalis  in,  212-214 
dyspnoea  in,  197 
etiology  of,  164 
inspection  of  chest  in,  194-195 
jugular  pulse  in,  129 
liver  in,  198 

myocarditis  and,  194-205 
nitroglycerine  in,  219 
pathology  of,  164 
precordial  pains  in,  197 
prognosis  in,  199-200  ff . 
prognostic   importance    of    acute    acci- 
dents in,  201-203 

cerebral  hemorrhage  in,  202 

clinical  history  in,  200 

coronary  disease  in,  203 

hypertension  in,  204 

hypertrophy  in,  203-204 

myocardial     insufficiency     in,      199, 
200-201 

pneumonia  in,  202 

pulmonary  stasis,  202 

uremia  in,  204 
pulmonary  symptoms  of,  198 
ventricular  fibrillation  in,  203 
Cardiosclerosis,  Acute  Accidents  in 
prognostic  significance  of,  201 
relation    of    cardiac    hypertrophy    to, 

203-204 
types  of,  201-203 
Cardiosclerosis,  Senile 
arrhythmias  in,  98-99 
blood  pressure  in,  267 
digitalis  in,  212 
precordial  pains  in,  267 
symptoms  of,  267 
therapy  of,  267 
Cardiovascular  Disease 

blood   pressure   in   hypertensive,    246- 

247 
blood  pressure  in  organic,  246—248 
caused  by  pneumonia,  154-155 
caused  by  pyorrhea,  157 
etiology  of,  149-159 
pathology  of,  164 
Cardiovascular    Disease    with    Hyper- 
tension and  Myocarditis 
blood  pressure  in,  246-247 
heart  changes  in,  247-261 
pathological  basis  of,  246-247 


Cardiovascular    Disease    with    Hyper- 
tension and  Myocarditis  (Continued) 

precordial  pains  in,  260-262 

symptoms  of,  261 

therapy  of,  261,  262 
Carotid  Pulse 

clinical  significance  of,  130 

in  aortal  disease,  130 

in  aortic  aneurismal  dilatation,  186 

in  aortic  regurgitant  lesions,  130 

in  aortitis,  130 

in  arteriosclerosis,  195 

in  extrasystole,  54 

in  hypertension,  130 

in  tachycardia,  130 
Carotid  Wave  in  Polygram,  15 
Cerebellar  Pressure 

and  extrasystoles,  97 

and  heart  block,  102 
Cerebral  Anemia 

blood  pressure  in,  249 

in  aortic  stenosis,  172 

intracranial  tension  and,  249 

symptoms  of,  249 
Cerebral  Circulation 

interference    of,    causing   heart   block, 
102 
Cerebral  Hemorrhage 

in  cardiosclerosis,  202 

in  hypertension,  204 

in  streptococcus  viridans,  178 

intracranial  tension  and,  249 
Cerebral  Lesions 

in  streptococcus  viridans,  178 
Cerebral  Pressure,  Increased 

and  extrasystoles,  97 

and  heart  block,  102 
Cerebral  Tumors 

causing  intracranial  tension  and  hyper- 
tension, 249 
Chloral 

in  acute  rheumatic  endocarditis,  174 
Codeine 

in  aneurismal  dilatation  of  aorta,  192 

in  tachycardia,  106 
Cohn,  A.  E.,  28,  47,  274 
Colloidal  Silver  Salts 

action  of,  222-223 

in  endocarditis,  222-223 
Colorimeters,  231 
Compensatory  Pause 

absence  of,  52 

after  extrasystole,  52,  54,  70 

in  paroxysmal  auricular  tachycardia,  56 

in  ventricular  escape,  74 
Complex,  Notched 

cause  of,  34,  35 

significance  of,  35,  36 
Conduction  System 

see    auriculo-ventricular  conduc- 
TION System 
Conduction  Time 

classification,  48 


INDEX 


285 


Conduction  Time  (Continued) 

etiology  of  prolonged,  83,  84,  103-104, 
206 

in  acute  endocarditis,  166 

in  auricular  extrasystole,  51-52 

in  auricular  flutter,  65 

in  exophthalmic  goiter,  55 

occurrence  of  prolonged,  103-104 

shortened,  84,  104 

therapy  of  prolonged,  104 
Conductivity  of  Cardiac  Musculature, 

4 
Congenital  Cardiac  Disease 

orthodiascopy  in,  122-128 

relation  to  length  of  life,  128 

types  of,  122-128 

with  right  ventricular  hypertrophy,  33 
Contractility  of  Cardiac  Musculature, 
4 

effect  on  T  wave,  45 

electric  reaction  produced  by,  22 

in  functional  efficiency  tests,  236 

relation  to  electric  excitation,  27 
Contractions,  Ectopic 

differentiation  from  extrasystole,  62 

differentiation  from  normal,  52 

in  auricular  fibrillation,  62,  63,  64 

in  normal  rhythm,  51 
Copper 

action  of,  150 
Coronary  Artery 

auricular  fibrillation  in  thrombosis  of, 
105 

disease  of,  149 

embolism,  auricular  fibrillation  in,    105 

embolism  of,   203,   264-265 

effect  of  nicotine  on,  268 

effect  of  nitroglycerine  on,  219 

heart  block  and  disease  of,  101 

in  cardiosclerosis,  164,  203 

infarction  of,  203,  264-265 

precordial  pains  in,  264-265 

relation  to  coronary  plexuses,  5 

relation  to  supply  of    A-V  conduction 
system,  9,  10 
Coronary  Disease 

course  of,  203 

endarteritis  and,  163 

precordial  pains  in,  203 

prognosis  in,  203 

symptoms  of,  203 

with  arteriosclerosis,  203 
Coronary  Sinus,  1 
Coupled  Rhythm 

caused  by  digitalis,  206,  211-212 

definition  of,  48 

diagnosis  of,  54 

electrocardiogram  of,  73-74 

method    of   estimating   blood  pressure 
in,  250 
Crises 

cause  of,  99 

in  pneumonia,  275 


Cyanosis 

blood  in,  168-169 

blood  pressure  in,  246,  249 

effect   of   digitalis   on,    211,    213,    246, 

249 
effect  of  strophanthin  on,  215 
in  decompensated  mitral  regurgitation, 

170 
in  diphtheria,  152 
in  patent  foramen  ovale,  127 
in  patent  interventricular  septum,  126 
in  pneumonia,  275 

in  pregnancy  with  cardiac  failure,  238 
Karrell  diet  in,  218-219 
Nauheim  baths  in,  226 
tricuspid  murmur  in,  142 
venesection  in,  249,  275 
with  dyspnoea,  168,  169 
without  dyspnoea,  169 

Decompensation 

blood  pressure  in,  246 

causes  of,  167-168 

digitalis  in,  174,  214 

extrasystoles  and,  97 

in   aneurismal   aortic   dilatation,    189- 
190 

in  aortic  stenosis,  172 

induction  of  premature  labor  in,  240- 
241 

in  mitral  regurgitation,  170 

in  streptococcus  viridans,  180-181 

jugular  pulsation  in,  121 

massage  in,  223 

passive  motion  in,  223 

pregnancy  and,  238 

with  wide  R,  37 
Depressor  Nerve 

relation  to  blood  pressure,  242-243 
Derivations 

See  Leads 
Dextrocardia,  Acquired 

cause  of,  30 
Dextrocardia,  Congenital 

classification,  28 

clinical  recognition  of,  30 

differentiated    from    acquired    dextro- 
cardia, 32 

effect  on  electrocardiogram,    30 
Diabetes 

cardio-vascular  symptoms  in,  151 

effect  on  heart,  151 

therapy,  151 
Diaphragm 

in  normal  orthodiascopic  tracing,    111— 
113 

in  squatty  heart,  28 

mobility  of,  113,  114,  138 
Diastolic  Period 

effect  of  digitalis  on,  213 

h  wave  in,  17 

in  sinus  arrhythmia,  82 

in  tachycardia,    55 


286 


INDEX 


Diastolic  Pressure 

as  index  of  cardiac  and  cerebral  disease, 
247 

in  uremia,  204,  247 

normal,  245 
Diathermy 

effect  on  blood  pressure,  253,  261 
Dicrotic  Notch 

cause  of,  19 

height  of,  20 
Dicrotic  Wave 

cause  of,  19 

notching  of,  19 
Diet 

in  cardio-renal  disease,   230-233 

in  compensated   valvular   disease,   229 

in  myocardial  insufficiency,  230,  263 

in  precordial  pains  of  gastric  origin,  269 

in  uremia,  262-263 

Karrell  —  see  Karrell  Diet 

Mosenthal's  nephritic  test,  231-232 

Schlayer's,  231 
Digitalis 

action    on    arrhythmias    by,    206-209, 
211-215 

arrhythmias  from,  198,  206-207 

atropine   sulphate   and,   206,   209-210, 
215 

bradycardia  from,  100 

compared    with    crystalline    strophan- 
thin,  215-216 

compared    with    theobromine    sodium 
salycilate,  217 

compensation  and,  237 

coupled  rhythm  from,  206,  211-212 

cumulative  effect  of,  212 

danger  of  overdose  of,  212-213 

dosage  of,  210-212 

duration  of  action  of,  212 

effect    on    blood    pressure,    192,    213, 
246,  261-262 

effect  on  heart,  45-46,  208-209,  215 

effect  on  heart  murmurs,  140,  141 

effect  on  T  wave,  45,  46,  274 

effect  on  ventricular  action,  206,  211,  213 

effects,  summary  of,  215 

extrasystoles  from,  99,  206,  207 

heart  block  from,  90 

hunger  pangs  caused  by,  207,  215 

hypersensitiveness  to,  207 

in  acute  endocarditis,  213-214 

in  aneurismal  aortic  dilatation,   192 

in  aortic  lesions,  213,  214 

in    auricular    fibrillation,    62-64,    105, 
206,  207,  210-211,  237 

in  auricular  flutter,  66,  107,  207 

in  cardiac  syphilis,  266 

in  cardiosclerosis,  212-214 

in  chronic  pericarditis,  214 

in  coronary  disease,  213 

in  cyanosis,  211-213,  246,  249 

in    decompensated  cardiovascular    dis- 
ease, 214-215 


Digitalis  (Continued) 

in  decompensated  mitral  stenosis,  174 

in     decompensated     valvular     disease, 
214-215 

in  decompensation,  174 

in  febrile  diseases,  214 

in     hypertensive     myocardial     insuffi- 
ciency, 262 

in  mitral  lesions,  213,  214 

in  non-hypertensive  myocardial  insuffi- 
ciency, 263 

in  pericarditis,  213-214 

in  pneumonia,  273-274 

in  premature  arteriosclerosis,  267 

in  senile  arteriosclerosis,  267 

in  senile  cardiosclerosis,  267 

in  treatment  of  extrasystoles,  99,  207 

in  treatment  of  heart  block,  111,     208- 
209 

in  treatment  of  tachycardia,  106,  211- 
212,  214,  237 

in  valvular  lesions,  213-215 

Karrell  diet  and,  218-219 

preparations  of,  210 

prolonged  conduction    time    from,    83, 
103,  206 

pulse  alternation  from,  92,  206,  208 

sinus  arrhythmia  from,  206,  211 

symptoms  of  poisoning  by,  207 

vagus  inhibition  and,  207-215 

variability  in  absorption  of,  210,  212 

ventricular  fibrillation  and,  203,  213 

vomiting  from,  209-210,  211,  215 
Dilatation,  Cardiac 

cause  of,  168 
Diphtheria 

cardiac  irregularities  in,  152-153 

death  in,  153 

endocarditis  and,  152-153 

method  of  diagnosing  heart  conditions 
in,  152-153 

myocarditis  and,  152 
Drop  Heart  (see  also  Narrow  Heart) 

classification,  28 

clinical  recognition  of,  30,  115,  256 

description  of,  30. 
Dropsy 

calomel  in,  221 

theobromine  sodium  salicylate  in,  217 
"Duck-shaped"  Heart,  119 
Ductus  Arteriosus  (Ductus  Botalli) 

and  right  ventricular  hypertrophy,  33 

illustrative  cases,  125-126 

in  fetal  heart,  2 

orthodiascopy  of,  125-126 

palpation  in,  133 

symptoms  of  patent,  124,  125,  126 
Ductus  Botalli 

See  Ductus  Arteriosus 
Dyspnosa 

action  of  strophanthin  in,  215 

after  massage,  223 

after  passive  motion,  223 


INDEX 


287 


Dyspnoea  {Continued) 

and  polygraphic  registration,  13 

caused  by  diphtheria,  152 

in  cardiosclerosis,  168,  107,  200 

in  coronary  disease,  203 

in  pregnancy  with  cardiac  failure,  238, 

239 
in  premature  arteriosclerosis,  266 
in  uremia,  247,  262 
in  uremia  with  cardiosclerosis,  204 
Karrell  diet  in,  218-219 
Nauheim  baths  for,  226 
origin  of,  168 
relation  of  blood  to,  168 
with  anemia,  168 

with  aneurismal  aortic  dilatation,  190 
with  cardiac  syphilis,  184 
with  chronic  endocarditis,  170 
with  cyanosis,  168 

with    decompensated    mitral    regurgi- 
tation, 170 

Edema 

aneurismal  aortic  dilatation  and,  190 

aortic  regurgitation  and,  173 

blood  pressure  in,  244 

calomel  in  renal,  221-222 

cardiosclerosis  and,  198 

chronic  endocarditis  and,  169 

diet  in,  230 

endomyocardial  disease  with,  264 

hypertensive     precordial     pains    with, 
262 

Karrell  diet  in,  218-219,  230 

massage  in,  223 

Nauheim  baths  in,  226 

pregnancy  and,  238 

secondary  cardiac  syphilis  and,  184 
Einthoven,  23,  25,  26,  39,  40-43,  45 
Electric  Potential 

description  of,  27 

difference  in,  causing  deviations,  39 

effect  of  cardiac  displacement  on,  30 
Electrical  Axis  of  Heart 

electrocardiographic     deviations     and, 
39 

method  of  determining,  40 

significance  in  electrocardiogram,  23-27 
Electrical  Negativity,  27 
Electrocardiogram 

apical  negativity  in,  42 

auricular  complex  of,  25 

deviations  of,  39-40  ff. 

diphasic  curve  of,  23,  45 

effect  of  digitalis  on,  274 

effect  of  size  and  volume  of  heart  on, 
27-28 

leads  of,  25 

mathematical  basis  of,  39—43 

method  of  taking,  23-25 

monophasic  curve  in,  22,  27,  45 

P  wave  in,  26 

variations  from  normal,  26 


Electrocardiographic  Apparatus 

description  of,  24 

physiological  basis  of,  22-23 
Endocarditis 

acute  bacterial  (see  also  Endocarditis, 
Bacterial),  176 

alcohol  causing,  150 

auricular  flutter  in,  66,  107 

bacteria  causing,  156,  161-162 

bacterial  agents  causing,  152-157,  161— 
162 

chemical  agents  causing,  149-152 

classifications  of,  165 

diabetes  causing,   151 

digitalis  in,  213-214 

diphtheria  toxins  causing,  152-153 
etiology  of,  149-159 

extraction  of  teeth  for,  156-157,  227 

fever  in,  165-166 

gout  causing,  151 

inspection  of  apical  region  in,  131 

lead  poisoning  causing,  149,  150 

metallic  poisons  causing,  149-150 

mouth  infection  causing,  156-157 

murmur  in,   144 

pathology  of,  161-162 

phosphorous  poisoning  causing,  150 

pneumonia  as  cause  of,  153-155 

products  of  food  metabolism  causing, 
151-152 

prognosis  of  rheumatic,  174-176 

prolonged  conduction  time  in,  83 

pyogenic  abscesses  causing,  157 

pyorrhea  alveolaris  causing,  156-157 

rheumatism  causing,  155 

silver  salts  in,  222-223 

streptococcus  viridans  in,  177-182 

symptomatology  of  acute,  162,  166-167 

symptomatology  of  chronic,  162,  167- 
173 

symptomatology  of  subacute,  162 

symptoms  of  rheumatic,  165-166 

syphilis  and,  158-159 

tobacco  poisoning  causing,  150-151 

tonsillectomy  in,  226-227 

tonsillitis  causing,   155-156 

valves  affected  in,  158 

ventricular  dilatation  in,  34 
Endocarditis,  Acute  Rheumatic 

diagnosis  of,   167 

exacerbations  in,  264 

pains  in,  167,  264 

precordial  pains  in,  264 

silver  salts  in,  222-223 

symptoms  of,  166-167,  264 

therapy  of,  173-174,  264 
Endocarditis,  Bacterial 

bacteria  causing,  152-157,  161-162 

course  of,  177 

differentiation  from  rheumatic,  176 

effect  on  myocardium,  163-164 

origin  of,  176 

pathology  of,  161 


288 


INDEX 


Endocarditis,  Bacterial  (Continued) 

petechias  in,  177 

septic  infarcts  in,  177 

symptoms  in,  176-177 

tabulation  of  bacteria  in,  158 

valves  attacked  in,   158 
Endocarditis,    Chronic  Rheumatic 

aortic  regurgitation  in,  173 

cyanosis  in,  168-169 

decompensated  mitral  regurgitation  in, 
170 

decompensated  mitral  stenosis  in,  170- 
172 

decompensation  in,  170-173 

dyspncea  in,  168-169 

hemoptysis  in,  173 

precordial  pains  in,  169-170 

renal  involvement  in,  169 

streptococcus  viridans  in,  177,  222 

symptoms  in,  167-170 

therapy  of,  173-174 

visceral  congestion  in,  169 
Endocarditis,  Fibroplastic,  162 
Endocarditis,  Infectious,  176-177 
Endocarditis,  Malignant,  161,  176-177 
Endocarditis,  Productive,   161 
Endocarditis,  Rheumatic 

complications  of,  175 

diagnosis  of,  167 

differentiation    from    acute    bacterial, 
176 

endocardial  manifestations,  165-166 

exacerbations  of,  167 

marriage  of  women  with,  238 

myocarditis  and,  164 

pathology  of,  161 

prognosis  of  acute  and  subacute  stages 
of,  174-175 

prognosis  of  chronic,  175-176 

prognosis  of  quiescent,  175-176 

prolonged  conduction  time  in,  103 

rheumatic  manifestations  in,  165 

symptomatology  of,  165-167 

valvular  murmurs  in,  139 
Endocarditis,  Septic,  161,  176-177 
Endocarditis,  Simple,  161 
Endocarditis,  Ulcerative,  161-162,  176- 

177 
Endocarditis,  Verrucous,  161-162 
Endocardium 

artheromatous  changes  in,  160,  161 

cardiosclerosis,  164 

description  of,  2 

development  of,  1 

effect  of  lead  on,  149 

fatty  degeneration  of,  160,  161 

in  tertiary  cardiac  syphilis,  184 

sclerosis  of,  160,  161 

structure  of,  160,  161 
Enterorrhagia 

in  streptococcus  viridans,  180 
Epicardium 

description  of,  2 


Epigastric  Pain 

cause  of,  259,  260 

relation     to     precordial     pains,     259, 
260,  268-269 
Epigastric  Pulsation 

cause  of,  131,  132 

in  right  ventricular  hypertrophy,  205 

occurrence,  131 
Epilepsy 

bradycardia  in,  100 

extrasystoles  in,  99 
Epinephrin  in  Blood 

as  cause  of  hypertension,  260 
Erysipelas 

acute  bacterial  endocarditis  in,  177 
Erythrol  Tetranitrate 

for  hypertension,  252,  261 
Esophageal  Disease 

precordial  pains  in,  269-270 
Excitation  Wave,  Electric 

relation  to  muscle  contraction,  27 

relation  to  wide  R  wave,  37 
Excitation  Wave  in  Ventricle 

course  of,  detailed,  44-45 

course  of,  general,  42 

in  auricular  fibrillation,  104 

origin  of,  42 

retardation  of,  34-35 
Excitement 

blood  pressure  after,  246,  261 

in  hypertensive  precordial  pains,  261 

in  "weak"  heart,  256-257 
Exercise 

effect  on  T  wave,  46 

for  "weak"  heart,  257 

in  cardiac  disease,  235 

in  hypertension,  253,  261 

in  hypertension  with  precordial  pains, 
261 

in  non-hypertensive  myocardial  insuffi- 
ciency, 263 

necessity  for,  223 

systolic  pressure  after,  236-237,  246 
Exophthalmic  Goiter 

auricular  fibrillation  in,  63 

blood  pressure  in,  248 

cardiac  palpation  in,  132 

carotid  pulse  in,  130 

conduction  time  in,  55,  104 

normal  polygram  in,  18 

tachycardia  in,  106 

EXTRASYSTOLE 

abortive,  51,  52 

aconite  and,  220 

apical  inspection  in,  131 

bradycardia  and,  78 

bromides  in,  221,  269 

cardiac  palpation  in,  132 

change  to  auricular  fibrillation,  198 

clinical  recognition  of,  52-54 

compensatory  pause  and,  52 

course  in  heart  of,  71,  72 

defined,  48 


INDEX 


289 


Extraststole  (Continued) 

differentiation    from    auricular    flutter, 
67 

differentiation  from   blocked   auricular 
beat,  83 

differentiation     from     complete     heart 
block,  92 

differentiation     from     ectopic     beats, 
62,  63 

differentiation  from  normal  beat,  50 

diseases  accompanied  by,  97-99 

effect  of  digitalis  on,  198 

etiology  of,  97,  98,  99 

extracardiac  origin  of,  97,  98,  99 

frustrane,  51,  52,  54,  6-4 

heart  sounds  in,  54 

heterogenetic  contraction,  49 

impulse  formation  in,  49,  50 

in  acute  endocarditis,  166 

in  cardiosclerosis,  198,  202 

in     decompensated     mitral    regurgita- 
tion, 170 

in  diphtheria,  152 

in    paroxysmal    auricular    tachycardia, 
56 

in  pneumonia,  276 

in    precordial    pains    with    pulmonary 
crises,  270 

interpolated,  47 

irregularly  occurring,  54 

method   of   estimating   blood   pressure 
in,  250 

missed,  51 

multiple,  52,  90 

nodal,  47,  69,  74 

pathological  contraction,  49 

pulse  alternation  and,  92 

regularly  occurring,  73 

significance  of,  97 

tabagism  and,  151,  268 

therapy  of,  97,  99 
Extraststole,  Auricular 

classification,  47 

clinical  recognition  of,  51-52,  54 

compensatory  pause  in,  54 

conduction  time  in,  51-52 

differentiation  from  ventricular  extra- 
systole,  54 

ectopic  contractions,  51 

from  smoking,  268 

in  paroxysmal  tachycardia,  55 

lengthened  conduction  time  in,  83 

pause  after,  70 

with  auricular  fibrillation,  63 
Extraststole,  Ventricular 

cause  of,  69-70 

classification,  47 

clinical  recognition  of,  52,  54,  70,  71 

compensatory  pause  in,  54.  70 

differentiation  of  auricular  from,  54 

digitalis  and,  206 

electrocardiographic  types  of,  72 

fibrillation  and,  63 

U 


Extraststole,  Ventricular  (Continued) 
in  complete  heart  block,  90 
interpolated,  71 
jugular  pulse  in,  129 
rate  of,  50,  70 

Fahr  and  de  W.urt,  39 
Fahr  and  Weber,  42,  45 
Fatigue 

symptom  of  "weak"  heart,  255 
"Fattt"  Heart,  163 
Femoral  Artert 

blood  pressure  in,  248 

blood  pressure  in  aortic  regurgitation 
in,  248 
Fever 

auricular  fibrillation  from,  105 

murmurs  in,  144 

reduplicated  apical  impulse  in,  147 

rheumatic  endocarditis  and,  165,  167 

simple  tachycardia  in,  106 

streptococcus  viridans  and,  178-179 
Fibrillation 

See  Auricular  Fibrillation 

See  Ventricular  Fibrillation 
Fibrillation    Wave    of    Electrocardio- 
gram, 58,  60,  62 
Fluoroscopt 

for  determining  cardiac  efficiency,  236 

in  aortic  stenosis,  124 

in  extrasystole,  98 

in  patent  ductus  arteriosus,  126 

of  aneurismal  dilatation  of  aorta,  191, 
195 

of  apical  impulse,  147 

of  congenital  dextrocardia,  32 

of  drop  heart,  30,  256 

of  squatty  heart,  28 

of  ventricular  hypertrophy,  33 

of  ventricular  rocking  motion,  36 

of  "weak"  heart,  256 
Foramen  Ovale,  1,  2 
Foramen  Ovale,  Patent 

difficulty  of  diagnosis  of,  127 
Foxglove 

See  Digitalis 
Fright 

extrasystoles  from,  99 

simple  tachycardia  from,  106,  173 

"weak"  heart  and,  256-257 
Functional  Efficiency  Tests 

description  of,  236 

for  estimating   cardiac  reserve  power, 
236 

myocardial  insufficiency  and,  200,  201 

objections  to,  236-237 

Gall  Bladder,  Inflammation  of 

extrasystoles  in,  98 
Gallop  Rhtthm 

definition,    145 

presystolic,    146 


290 


INDEX 


Gangrene 

caused      by      streptococcus     viridans, 
179 
Gastric  Disturbances 

epigastric  distress  in,  268-269 

precordial  pains  in,  268-269 

therapy  of,  269 
Gastro-intestinal  Disease 

bradycardia  from,  99 

extrasystoles  from,  97 

simple  tachycardia  in,  106 
Gerhardt's  Area  of  Dullness 

in  patent  ductus  arteriosus,  125,  126 
Globular  Heart 

description,  117 

in  mitral  disease,  115-118 
Glucose  Solutions 

in  uremia,  263 
Goldscheider's   Ortho-Percussion 

See  Ortho-Percussion 
Gout 

endocarditis  from,  151 
Graphic  Methods 

advantages  of,  48 

limitations  of,  48 
Grippe 

digitalis  in,  214 

endocarditis  from,  156 

precordial  pains  in  crisis  of,  270 
Grcedel 

"duck-shaped"    heart,    117 

table  of  vertical  orthodiagrams,  113 

h   Wave,  17 

See  Poltgraphic  Tracing 
Headache 

in  cerebral  anemia,  249 

in  uremia,  204,  247,  262 
Head's  Zones 

epigastric,  259,  269 

in  cardiac  syphilis,  266 

in  endo-myocardial  disease,  264 

in  precordial  pains  in  respiratory 
affections,  270 

precordial  pains  and,  259,  264 
Heart 

anatomy  of,  2,  3,  4 

'arterial  supply  of,  3,  4 

conduction  system  (see  also  Auriculo- 
ventricular  Conduction  System), 
7-10 

contractility  of,  4 

development  of,  1 

displacement  of,  30 

effect  of  atropine  on,  45 

effect  of  digitalis  on,  45 

electrical  impulse,  27 

lymph  yessels  of,  4 

maximal  contraction  of,  4 

method  for  determining  outline  of, 
137 

musculature  of  (see  also  Musculature 
of  Heart),  4 


Heart  (Continued) 

nerve  supply  of,  4,  259 

physical  examination  of,  129-147 

physiology  of,  2,  3,  4 

position  of,  in  adults,  2 

position  of,  in  fetus,  1,  2 

sarcoplasm,  3 

size  of,  2 

types  of,  28-34 

weight  of,  in  adults,  2 
Heart  Block 

a  wave  in,  14 

auriculo-ventricular  ratio  in,  65 

cardiac  causes  of,  101 

cardiosclerosis  and,  198 

classification,  48 

clinical    and    experimental    causes    of, 
100 

clinical  recognition  of,  66,  67 

definition  of,  101 

differentiation  from  nutter,  67 

differentiation   from  true   bradycardia, 
79 

digitalis  in,  101,  206-208 

diphtheria  and,  152 

extracardiac  causes  of,  101-103 

inspection  of  apical  region  in,  131 

pneumonia  and,   153 

therapy  of,  101,  103 
Heart  Block,    Complete 

auricular  fibrillation  and,  67 

auricular  nutter  and,  64 

blood  pressure  in,  250 

classification,  48 

clinical  recognition  of,  36,  66,  91-92 

definition  of,  85 

differentiation  of  extrasystole  from,  92 

differentiation  of  incomplete  from,  129 

digitalis  in,  208 

etiology  of,  5 

jugular  pulsations  in,  129 

morphine  and,  221 

reflex  vagus  excitation  and,  103 

relation  to  M  and  W  waves,  35 

Tinct.  Squills  and,  216 

types  of,  36 

ventricular  rate  in,  91,  92 

wide  R  wave  and,  37 
Heart  Block,  Incomplete 

auricular  flutter  and,  64 

change  from  complete  to,  65,  66 

classification,    48 

clinical  recognition  of,  66,  85 

description  of,  85 

differentiation  of  complete  from,  129 

differentiation  of  nutter  from,  67 

differentiation   of   sino-auricular  from, 
92 

digitalis  in,  208 

types  of,  85 
Heart  Sounds 

auscultation  of,  138-147 

cardiac  palpation  and,  132-134 


INDEX 


291 


Heart  Sounds  (Continued) 

factors  influencing,  139 

gallop  rhythm  and,  145,  205 

in    aneurismal    aortic    dilatation,    185- 
186,  190 

in  aortitis,  195,  196 

in  complete  heart  block,  92 

in  extrasystole,  54,  83 

in  hypertension,  205,  261 

in  incomplete  heart  block,  92 

in  left  ventricular  hypertrophy,   204- 
205 

in    myocardial     insufficiency     without 
hypertension,  263 

in  myocarditis,  194,  195,  196 

in  senile  cardiosclerosis,  267 

normal,  analysis  of,   147 

reduplicated,  145-147 

reduplicated  apical  impulse  and,    147, 
205 

reduplicated  first  and,  146 

split,    canter,    double,    triple    rhythm 
and, 145 
Heart  Sounds,  Reduplicated  First 

etiology  of,  146 

in  aneurismal  dilatation  of  aorta,  186, 
190 

in  cardiosclerosis,  197 
Heart  Sounds,   Reduplicated  Second 

description  of,  146 

etiology  of,  145,  146 

in  mitral  stenosis,  146 

in  tachycardia,  146 

where  heard,  145 
Heart  Sound,  Third 

description  of,  145 

etiology  of,  145 
Hemiplegia 

in      decompensated      mitral     stenosis, 
172 

in  streptococcus  viridans,  180 
Hemoptysis 

cause  of,  173 

in  aortic  regurgitation,  173 

in  cardiosclerosis,  197-198 

in  decompensated  mitral  regurgitation, 
170 

in    pregnancy    with     cardiac     failure, 
238-239 
Heterogenetic  Contraction,  50 
Heubner's  Nodes,   179 
Homogenetic  Beat 

description  of,  48-49 

ectopic,  51 
Hydrocephalus 

causing  heart  block,  102 
Hydrotherapy 

for  neuropathic  individuals,  224-225 

hypertension  and,  252-253,  261-262 

procedure  in,  225 

types  of,  224,  252 
Hydrothorax 

in  cardiosclerosis,  198 


Hyperpiesis 

blood  pressure  in,  249 
definition  of,  249 
Hypertension 

adrenalin  in,  220 

alcoholism  and,  150 

aortitis  and,  195 

blood    pressure    in    (see    also    Blood 

Pressure),  247 
cardiac  palpation  in,  133-134,  138 
carotid  pulse  in,  130 
causes  of,  260-261 
cerebral  hemorrhage  in,  204 
cyanosis  causing,  249,  261 
diathermy  in,  253 
differentiation    between     cardiac     and 

cerebral  types  of,  247 
digitalis  in  cardiosclerotic,  213,  249 
drugs  in,  252 
exercise  in,  253 
heart  changes  in,  260-261 
heart  sounds  in,  195-196,  205 
hydrotherapy  in,  252-253 
Karrell  diet  in,  218-219 
left  ventricular  hypertrophy  in,  205,  261 
myocarditis  in,  246,  247,  260-261 
percussion  in,  253 
pneumonia  and,   154—155,  276 
prognosis  of  cardiosclerosis  with,  200, 

204 
Spa  treatment  for,  253 
therapeutics  of,  251-253,  261-262 
vasodilators  in,  252 
venesection  in,  252 
wide  R  wave  in,  37 
Hypertension,  Functional 

See  Hyperpiesis 
Hypotension 

adrenalin  in,  221 
blood  pressure  in,  249,  250 
in  "weak"  heart,  256,  257 
symptoms  of,  221,  250 

Idioventricular  Rate 

in  complete  heart  block,  85 
Impulse 

abnormal  passage  of,  47,  68 

apical  —  see  Impulse,  Apical 

electrical,  27 

in  bundle-branch  lesions,  77 

in  extrasystole,  48 

myogenic,  10 

neurogenic,  10 

normal,  course  of,  10 

origin  of,  7,  10 

relation  to  arrhythmias,  10 
Impulse,  Apical 

position  determined,  137 
Impulse,  Apical,  Reduplicated 

description  of,  146,  147 

diagnosis  of,  146 

electrocardiogram  and,  147 

etiology  of,  146-147 


292 


INDEX 


Impulse,  Apical,  Reduplicated  {Continued) 
occurrence  of,  146-147 
orthodiagraphy  of,  147 
right  ventricular  hypertrophy  and,  205 
Indigestion,  Acute 

causing  paroxysmal  tachycardia,  106 
Infarcts 

arrhythmias  in  cardiosclerotic,   202 
coronary,     result     of     cardiosclerosis, 

203,  264-265 
embolic,  in  pregnancy,  239 
heart  block  and,  101 
in  kidney,  178 

of  coronary  artery,  203,  264,  265 
precordial  pain  in  embolic  infarcts  of 

coronaries,  264-265 
rheumatic  endocarditis  and,  175 
septic,  in  acute  bacterial  endocarditis,  177 
Inspection  of  Cardiac  Area 
aortic  pulsation  and,  130 
apical  region  and,  130-131 
carotid  pulsation  and,  130 
epigastric  pulsation  and,  131,  132 
in  aortic  aneurismal  dilatation,  190 
jugular  pulsation  and,  129,  130 
liver  pulsation  and,  132 
right  lower  interspaces  and,  131 
supplemented    by    other    methods    of 

examination,  137 
value  of,  128 
Interpolation  Table,  40-43 
Intestinal  Disease 

causing  extr asystoles,  97 
Intracardiac  Ganglia,  5 
Intracranial  Tension 

blood  pressure  in,  249 
Iodide  of  Potash 

in  aneurismal  aortic  dilatation,  191 
in  hypertension,  252 
in  syphilitic  heart  block,  101 
Iso-Potential,  Line  of,  25 

Jaundice,  Catarrhal 

true  bradycardia  in,  99,  100 
Jugular  Bulb 

causing  split  a  wave,  16 

in  auricular  fibrillation,  58 

Mackenzie  polygraph  and,  13 
Jugular  Pulse 

auricular  systole  and,  129 

experimental  auricular  pressure  curves 
and  the  human,  14 

in  arrhythmias,  64 

in  auricular  fibrillation,  67,  129,  130 

in  auricular  flutter,  67,  130 

in  cardiosclerosis,  129 

in  complete  heart  block,  129 

in  decompensation,  129 

in  extrasystole,  54,  129 

in  incomplete  heart  block,  129 

in  tricuspid  regurgitation,  129 

normal  waves  in,  14 

position  of  patient  in  observing,  129 


Junctional  Tissue 

See  Auriculo-ventricular   Conduc- 
tion System 

Karrell  Diet 

cardiorenal  disease  and,  218 
description  of,  218 
edema  and,  218 
modification  of,  218-219 
myocardial  insufficiency  and,  218,  230 
with    theobromine    sodium    salicylate, 
217-218 

Lead  Poisoning 

action  of,  149 

blood  pressure  in,  248-249 

bradycardia  in,  99 

diagnosis  of,  149-150 

endocarditis  from,  149-150 
Leads,  Electrocardiographic 

cardiac  displacement  and,  30 

congenital  dextrocardia  and,  30 

definition  of,  25 

electric  axis  and,  39 

phasic  respiratory  variation  and,  32 
Lesions,      Stenotic     (see      also     Mitral 
Stenosis,    and    Aortic    Stenosis), 
139-142 
Lewis,  T.,  64,  71,  76 
Liver 

epigastric  pains  from  enlarged,  259 

in  cardiosclerosis,  198 

in  chronic  rheumatic  endocarditis,  169 

in  decompensated  mitral  stenosis,  170 

in  pregnancy  with  cardiac  failure,  238 
Liver  Pulsation 

importance  of,  132 

in  decompensated  mitral  stenosis,   170 

in  regurgitant  valvular  lesions,  141,  144 

in  stenotic  valvular  lesions,  142 

occurrence  of,  132 

M   Complex 

cause  and  description  of,  35 

clinical  significance  of,  35,  36 

myocarditis    with    double    apical    im- 
pulse and,  147 

rocking  motion  of  ventricle  and,  34 
Mackenzie 

polygraph  of,  12 

"youthful  irregularity"  of,  79 
Maladie  de  Hodgson,  185 
Mannitol 

in  hypertension,  252 
Marriage    of    Women    with    Valvular 

Disease,  237,  241 
Massage 

advantages  of,  223 

cardiac  decompensation  and,  223 

method  of  administration  of,  223-224 

necessity  for,  223 
Meningitis 

heart  block  and,  102 


INDEX 


293 


Meningitis  {Continued) 

in  acute  bacterial  endocarditis,  177 

increased     intracranial     tension     and, 
249 

streptococcus  viridans  and,  180 
Menopause 

treatment  of  precordial  pains  in,  270 
Mercury 

action  on  kidneys,  150 

in  aneurismal  aortic  dilatation,  191 
Metabolism,  Food 

causing  cardiac  disease,    151-152 
Metallic  Poisons 

causing  endocarditis,  149-150 
Mitral  Lesion 

auricular  fibrillation  in,  115—118 

blood  pressure  in,  248 

chest  palpation  in,  133,  134,  138 

combined  aortic  and,  120,  248 

cyanosis  in,  169 

digitalis  in,  213,  215 

hemic  murmurs  and,  145 

inspection  of  apical  region  in,  131 

liver  pulsation  in,  132 

low  dicrotic  notch  in,  20 

normal  polygram  with,  17 

orthodiagrams  of,  105-107,  115—118 

regurgitant  murmur  in,  139,  145 
Mitral  Regurgitation 

causes  of,  142 

cause  of  murmurs  in,  144 

decompensation  in  chronic  rheumatic, 
170-172 

differentiation  of  non-organic  murmur 
from,  144 

double  aortic  lesion  and,  120 

liver  pulsation  in,  132 

murmurs  in,  196 

normal  polygram  in,  17 

orthodiagrams  of,  118 

pregnancy  and,  239 

symptoms  of  decompensation  in  chronic 
rheumatic,  170 

syphilis  and,  159 

tonsillitis  and,  156 

verrucous  endocarditis  and,  162 
Mitral  Ring 

dilatation  of,  causing  murmurs,  144 
Mitral  Stenosis 

acute  rheumatic  endocarditis  and,     364 

apical  inspection  in,  130 

auricular    fibrillation    in,    56,    58,    60, 
104,  105,  172 

chest  palpation  in,  134 

decompensated,    in    chronic    rheumatic 
endocarditis,  170-172 

definition  of,  139 

jugular  pulsation  in,  129 

length  of  life  in,  176 

murmurs  of,  139-142 

normal  polygram  in,  17 

paralysis    of   left    recurrent    nerve    in, 
170-172 


Mitral  Stenosis  {Continued) 

pregnancy  and,  239 

reduplicated  2d  heart  sound  in,  146 

right  ventricular  hypertrophy  and,  33 

symptoms  of  decompensated,   170-172 

verrucous  endocarditis  and,   162 
Mitral  Valves 

auricular  fibrillation  and,  58 

bacteria  affecting,  158 

blood  vessels  in,  160 

cardiosclerosis  and,  164 

fatty  degeneration  of,  160-161 

position  of,  2 

relative  insufficiency  of,  143 

sclerosis  of  endocardium  and,  160—161 

streptococcus  viridans  and,  177-178 

tertiary  cardiac  syphilis  and,  184 
Moderator  Band,  9 
Monoplegia 

in  streptococcus  viridans,  180 
Morphine 

complete  heart  block  from,  101,  221 

effect  on  heart  rate  of,  221 

in  aneurismal  aortic  dilatation,  192 

in  auricular  fibrillation,  105 

in  hypertensive  precordial  pains,  261 

in  paroxysmal  tachycardia,  106 
Murmur,  Functional 

characteristics  of,  143 

definition  of,  143 

differentiation  of  organic  from,  144 

etiology-  of,  143-144 

in  anemia,  145 

occurrence  of,  143 
Murmur,  Machinery 

definition  of,  125 

in  patent  ductus  arteriosus,  125 
Murmurs  {see  also  Murmurs,  Machinery, 
Hemic,  and  Functional) 

atherosclerosis  and,  142—143 

auriculo-systolic,  139 

Austin  Flint,  141 

cardio-pulmonary,  145 

cardio-respiratory,  145 

definition  of,  139 

differentiation  between  typical  organic 
and  non-organic,  144-145 

effect  of  digitalis  on,  140—141 

endocardial,  175,  179 

extracardiac,     of     non-organic     origin, 
145 

Graham-Steele,  139 

hemic,  143,  144 

importance  of,  in  diagnosis,  139 

in  aortic  regurgitation,  141 

in  aortic  stenosis,  141 

in  aortitis,  195-196 

in  anemia,  143—145 

in  aneurismal  dilatation  of  aorta,   186, 
190 

in  auricular  fibrillation,  140 

in  degenerative  endocarditis,  161 

in  fibrillation,  60 


294 


INDEX 


Murmurs  (Continued) 

in  mitral  regurgitation,  139,  144 

in  mitral  stenosis,  139-141 

in    myocardial     insufficiency    without 
hypertension,  263 

in  myocarditis,  144,  195-196 

in  pregnancy  with  cardiac  lesions,  238 

in  patent  ductus  arteriosus,  125 

in  patent  foramen  ovale,  127 

in  secondary  cardiac  syphilis,  184 

in  streptococcus  viridans,    181 

in  third  heart  sound,  145 

in    tricuspid    valvular     lesions,     141- 
142,  144 

in  valvular  lesions,  142 

in    valvular    pulmonary    insufficiency, 
142 

in   "weak"   heart,   256 

influence  of  patient's  position  on,  139 

intracardiac,     of     non-organic     origin, 
143-145 

methods  of  determining  type  of,  143 

organic  valvular,  139-142 

reduplicated  apical  impulses  and,  145- 
147 

reduplicated  sounds  and,  145-147 

systolic,  108 

systolic,  in  patent  ductus  arteriosus,  124 

systolic,     in     patent     interventricular 
septum,  126 

valvular,  in  rheumatic  endocarditis,  139 

valvular  lesions  and,  142 
Musculature,  Cardiac 

attributes  of,  4,  259 

conductivity  of  (see  Conductivity) 

contractility  of  (see  Contractility) 

effect  of  pneumonia  on,  153-154 

electrocardiogram  and,  27-28 

fetal  development  of,  1 

fibres  of,  3 

in  heart  block,  101 

in  syphilis,  158 

irritability  of,  4 

pulse  alternation  and,  92 

superficial  bulbo-spinal  fibres  of,  3 

superficial  sino-spinal  fibres  of,  3 
Myalgia,  271 

Myocardial  Insufficiency  (see  also  Myo- 
carditis, Cardiosclerosis,  and  De- 
compensation) 

adrenalin  in,  221 

blood  pressure  in,  247-248 

diet  in,  230 

dyspnoea  in,  169,  200-201 

pathological  damage  in,  200-201 

precordial  pains  in,  200-201 

prognosis  in,  200-201 

therapy  of,  201 

valvular  disease  and,  248 
Myocardial  Insufficiency    with  Hyper- 
tension   and    Labile    Vasomotor 
Mechanism 

blood  pressure  in,  247 


Myocardial  Insufficiency  with  Hyper- 
tension and  Labile  Vasomotor 
Mechanism  (Continued) 

precordial  pains  in,  262 

symptoms  of,  247,  262 

therapy  of,  262 

vasodilators  in,  252 
Myocarditis  (see  also  Cardiosclerosis) 

acute  interstitial,  163,  164 

blood  pressure  in,  246-248 

bundle  lesions  in,  146 

chest  palpation  in,  131 

diabetes  and,  151 

diagnosis  of,  194-197 

differentiation  of  aneurism  from,  196 

embolic  coronary  infarcts  in,  265 

evidences  of,  98 

fibrous  interstitial,  164 

from  alcohol  poisoning,  150 

from  lead  poisoning,  150 

heart  sounds  in,  194-197 

hypertrophy  and,  204-205,  247 

murmurs  in,  144,  146,  194,  195-196 

orthodiascopy  in,  263 

other  lesions  and,  194 

precordial  pains  in,  263,  264 

prolonged     conduction    time     in,     83, 
104 

pulse  alternation  in,  92 

pyorrhea  and,  156 

physical  signs  of,  194,  204-205 

R  wave  in,  37-38 

reduplicated  apical  impulse  in,  147 

rheumatic  endocarditis  and,  164 

rheumatism  and,  155 

symptoms  of,  263 

syphilis  and,  159 

T  wave  in,  45 

tertiary  cardiac  syphilis  and,  185 

therapy  of,  263,  264 

ulcerative,  164 

ventricular  extrasystoles  in,  83 
Myocardium 

abcesses  in,  163-164 

anemic  necrosis  of,  163 

atrophy  of,  162 

bacterial  infection  of,  163-164 

brown  atrophy  of,  162 

cardiac  syphilis  and,  184-185 

cardiosclerosis  and,  164 

circulatory  disturbances  and,  163 

effect  of  diphtheria  on,  152-153 

effect  of  pneumonia  on,  153 

fatty  degeneration  of,  162-163 

parenchymatous  degeneration  of,  162 

simple  atrophy  of,  162 

Narrow  Heart  (see  also  Drop  Heart) 

description  of,  114,  115 

orthodiascopic  tracing  of,  113,  114 

symptoms  of,  115 
Nauheim  Baths 

benefits  of,  226,  253 


INDEX 


295 


Nauheim  Baths  (Continued) 

for  hypertension  with  precordial  pains, 
261 

method  of  producing,  at  home,  226 

routine  at  Spa,  226 

types  of  patients  suitable  for,  226 
Nausea 

in  cardiosclerosis,  204 

in  uremia,  247,  262 
Nephritis 

acidosis  in,  233-234 

aortitis  and,  121 

chemical  examination  of  blood  in,  233- 
234 

diabetes  and,  155 

diet  in,  233 

effect  of  caffein  in,  216 

effect    of    theobromine    sodium    salic- 
ylate in,  217 

functional  efficiency  tests  in,  230-233 

lactose  test  in,  230 

lead  poisoning  and,  149 

non-protein  nitrogen  in  blood  in,  233- 
234 

phenolsulphophthalein  test  in,  230-231 

prolonged    conduction    time    in,    103- 
104 

streptococcus  viridans  and,  178 

test  diet  in,  232 
Nerve,  Paralysis  of  Left  Recurrent 

relation  to  mitral  stenosis,  170-172 
Nerve  Plexuses  of  Heart 

A-V  system  and,  10 

coronary,  5 

deep  cardiac,  4,  5 

sino-auricular  node  and,  7 

superficial,  4,  5 
Nerves 

in  aneurismal  dilatation  of  aorta,  189 

in  streptococcus  viridans  infection,  180 
Nerves  of  Heart 

auriculo-ventricular     system     and,     9, 
10,  259 

blood  pressure  and,  242,  243 

cervical  plexus  and,  5 

dorsal  plexus  and,  5 

gastric  nerves  and,  98,  259,  260   3 

plexuses  of,  4,  5 

premature  contractions  and,  50 

sensation  and,  259 

sensory,  5 

sympathetic  system  and,  5,  7,  151,  259 

tone  of,  5 
Neuralgia 

in  aneurismal  dilatation  of  descending 
aorta,  189 

precordial,  270-271 
Neurasthenic       Heart,     see      "Weak" 

Heart 
Neurotic  Heart,  see  "Weak"  Heart 
Nicotine  (see  also  Tabagism) 

effect  on  sympathetic  ganglia,  83 

precordial  pains  from,  268 


Nitrites 

dose  of,  219 

in  hypertension  with  precordial  pains, 
261 

uses  of,  219 
Nitroglycerine 

blood  pressure  and,  219,  261 

dose  of,  219,  252 

in  cardiosclerosis,  219 

in  hypertension,  252,  262 

in  pulmonary  edema,  219 

in  tabagism,  268 

in  "weak"  heart,  257 

precordial  pains  and,  219,  261,  270 
Nodal  Rhythm,  56 
Node  of  Keith-Flack,  see  Sino-auricular 

Node 
Node  of  Tawara,  see  Atrio-ventricular 

Node 

Occupation 

for  patients  with  cardiac  disease,  235- 

236 
Oertel  Treatment,  224 
Oliguria 

in  cardiosclerosis  with  uremia,  204 
Orthodiascope    Tracing 

description  of  normal,   111,   112 
factors  influencing  size  of,  113,  114 
in  aneurismal  dilatation  of  aorta,  185, 

195 
in  aortic  stenosis,  122,  124 
in  aortic  valvular  lesions,  118,  119 
in  aortitis,  120-122 
in  combined  aortic  and  mitral  disease, 

120 
in    congenital    cardiac    malformations, 

122-128 
in  mitral  disease,  115-118 
in  myocardial  insufficiency,  263 
in  patent  ductus  arteriosus,  124-126 
in  patent  foramen  ovale,  127-128 
in     patent     interventricular     septum, 

126-127 
in  rheumatic  aortic  disease,  118-120 
influence  of  diaphragm  on,  114 
measurements  of,  113 
of  broad  heart,  113-114 
of  narrow  heart,  113-114 
standards  in,  112-114 
Orthodiascopy  (see  also   Orthodiascope 

Tracing) 
cardiac  efficiency  and,  236 
definition  of,  110 
description     of     Groedel     Apparatus, 

110,  111 
in  mitral  disease,  115-118 
method  of  using,  111 
percussion,   compared  with,    134,    135, 

137,  138 
roentgenograph^  distortion  and,  110 
Orthopercussion 

description  of,  135 


296 


INDEX 


Ostium  Venosum,  3 
Ovarian  Extract 

for  "weak"  heart  at  menopause,  257, 
270 
Overstrain 

causing  simple  tachycardia,  106 
causing  ventricular  dilatation,  34 
Oxygen   Baths,   see  Hydrotherapy,  and 
Baths,  Carbon  Dioxide 

P  Wave  of  Electrocardiogram 

cause  of,  26 

description  of,  26 

in  auricular  extrasystole,  52 

in  auricular  fibrillation,  62 

in  auricular  flutter,  66 

in  nodal  extrasystole,  69 

in  ventricular  extrasystole,  72 

notched,  36 

variations  of  normal,  26 
Pacemaker,  see  Sino-auricular  Node 
Palpation  of  Chest 

aorta  in,  133 

diagnostic  value  of,  129,  132,  133 

in  aneurism,  133 

in  aneurismal  dilatation  of  aorta,  133, 
190 

in  aortitis,  133 

in  arteriosclerosis,  133 

in  auricular  fibrillation,  133 

in  cardiosclerosis,  195 

in    congenital    patent    interventricular 
septum,  133 

in  congenital  pulmonary  stenosis,  133 

in  extrasystoles,  132 

in  hypertension,  133 

in  mitral  lesions,  134 

in  mitral  stenosis,  133 

in  overacting  pulmonary  arteries,  133 

in  patent  ductus  arteriosus,  133 

in  pulsus  paradoxus,  134 

in  reduplicated  apical  impulse,  146 

in  rheumatic  aortic  stenosis,  133 

in  rheumatic  regurgitant  lesions,  133 

in  tachycardia,  134 

over  base  of  heart,  133 

supplemented    by    other    methods    of 
examination,  137 
Papillary  Muscle 

excitation  wave  in,  44 
Passive  Motion 

method  of  administration  of,  223-224 

use  of,  223 
Patent  Interventricular  Septum 

chest  palpation  in,  133 

clinical  evidences  of,  126 

orthodiascopy  of,  126-127 
Percussion 

auscultatory,  135,  191 

inaccuracy  of,  135,  137 

in  aneurismal  dilatation  of  aorta,    190- 
191 

ortho-percussion,    135 


Percussion  (Continued) 

spinal,  253 

value  of,  129 
Percussion  Wave,  see  Primary  Wave 
Pericarditis 

cause  of,  163-164 

digitalis  and,  214 

in    pregnancy     with     cardiac    lesions, 
'  238 

precordial  pains  in,  271 

pulsus  paradoxus  in,  92 
Peripheral  Resistance 

mechanism  of,  242-243 

relation  to  blood  pressure,  242-243 
Peritonitis 

extrasystoles  in,  98 
Petechia 

description  of,  179 

in  acute  bacterial  endocarditis,  177 

in  conjunctivae,  179 

in  skin,  179 

in  streptococcus  viridans,  179 
Phasic  Variation  with  Breathing 

apical  inspection  in,  131 

cause  of,  32 

classification,  28 

compared   to  rocking  motion  of  ven- 
tricle, 34 

description  of,  32 

effect    on    cardio-respiratory    murmur, 
145 

in  sinus  arrhythmia,  79,  82 

in  ventricular  hypertrophy,  32 
Phenolsulphophthalein  Test 

in  chronic  endocarditis,  169 

in  nephritis,  230-231 

in  uremia,  247 
Phlebogram  (see  also  Jugular  Pulse  and 
a-c-v  Waves) 

normal,  15 

of  nodal  extrasystole,  69 

variations  in  normal,  16-17 
Phosphorus  Poisoning 

endocarditis  from,  150 

fatty     degeneration     of     myocardium 
from,  163 
Physiological  Beat,  48-59 

relation  to  extrasystoles,  50 
Pleural  Exudates 

causing  heart  displacement,  30 
Pleurisy 

precordial  pains  in,  271 
Pneumonia 

acute  bacterial  endocarditis  in,  176 

area  of  involvement  in,  274—275 

auricular  fibrillation  in,  63 

bradycardia  in,  100 

cardiac  musculature  and,  153-155 

cardiosclerosis  from,  154-155 

cardiovascular  disease  from,  154—155 

cause  of  death  in,  154 

crisis  in,  275-277 

critical  resolution  in,  275-276 


INDEX 


297 


Pneumonia  (Continued) 

digitalis  in,  214,  274-276 

drugs  in,  273-276 

endocarditis  from,  153-155 

extrasystoles  in,  98-99 

expectoration  at  crisis  in,  275 

hypertension  from,  154-155 

in  cardiosclerosis,  202 

late  sequelae  of,  154-155 

myocarditis  from,  153,  274 

nephritis  from,  155 

stimulation  in,  273-276 

temporary     auricular     fibrillation    in, 
105 

therapy  of,  273-277 

toxic  cases  of,  274 

toxins  in,  102,  153-155,  274 

variety  of  treatments  for,  273 

venesection  in,  274-275 

ventricular  arrhythmias  and,  68 
Poisons,  Chemical 

causing  heart  block,  102 
Polygraph 

description  of,  12 

limitations  of,  17 

method  of  use  of,  13,  14 

tracings,  13,  20 

uses  of,  12,  14 
Potash  and  Soda,  Acetate  of 

dose  of,  221 

effect  of,  221 
Potential      Differences  —  Table      of, 

40-43 
Precordial    Neuralgias    (see    also    Pre- 
cordial Pains),  270-271 
Precordial  Pains 

areas  affected  in,  259 

etiology  of,  260 

Head's  zones  in,  259,  264,  266 

importance  of  cardiac  history  in,  258, 
259 

in  acute  pulmonary  crisis,  270 

in  acute  rheumatic  endocarditis,    167, 
264 

in  aortic  regurgitation,  173 

in  arteriosclerosis,  266,  267 

in  cardiac  syphilis,  184,  266 

in  cardiosclerosis,  197,  200,  267 

in  chronic  rheumatic  endocarditis,  169- 
170 

in  coronary  disease,  203 

in  decompensated  mitral  stenosis,  170 

in  embolic  infarcts  of  coronaries,  264— 
266 

in  esophageal  disease,  269-270 

in  gastric  disturbances,  268-269 

in  hypertensive  cardiovascular  disease, 
260-262 

in    myocardial     insufficiency    without 
hypertension,  263-264 

in  sacculated  aneurisms,  267 

in  tabagism,  268 

in  uremia,  247,  262-263 


Precordial  Pains  (Continued) 

neuralgia,  271-272 

nitroglycerine  for,  219 

pathology,  258-260 

relation  to  cardiovascular  nerve  supply, 
259 

relation   to   epigastric   pains,    259-260, 
268-269 

sub-sternal,  189 

therapy  of,  261-271 

use  of  term  —  angina  pectoris,  instead 
of,  258 

with  vasomotor  disturbances  at  meno- 
pause, 270 
Predicrotic  Wave,  see  Systolic  Wave 
Pregnancy 

abortion  in,  240 

aortic  lesions  in,  239-240 

decompensated  endocardial  lesions  in, 
240-241 

in  women  with   cardiac   disease,    238- 
241 

with  valvular  lesions,  238-239 
Premature  Beats,  see  Extrasystole 
Presystolic  Wave,  60 
Primary  Wave  of  Radial  Tracing,  18 
Proteins 

effect  on  cardiovascular  system,  152 
Pulmonary  Artery 

congenital  malformation  of,  33 

development  of,  1,2 

orthodiascopic  tracing  of,  111,  112 
Pulmonary  Disease 

dyspnoea  and  tachycardia  in,  106 

precordial  pains  in,  270 
Pulmonary  Edema 

coronary  disease  and,  203 

in  pneumonic  crisis,  275 

nitroglycerine  in,  219 

relation  of  expectoration  to,  275 
Pulmonary  Stasis 

in  cardiosclerosis,  202 
Pulmonary  Stenosis,  Congenital 

chest  palpation  in,  133 

differentiation  of  aortic  from,  142 

murmurs  in,  142 
Pulmonic  Sound,  Second 

in  right  ventricular  hypertrophy,  205 
Pulmonary  Valves 

insufficiency  of,  142,  144 

position  of,  2 

reduplicated  second  heart  sounds  and, 
146 
Pulse 

anacrotic,  20 

bisferiens,  20 

collapsing,  20 

Corrigan,  20 

dicrotic,  20 

hard,  20 

hyperdicrotic,  20 

in  auricular  fibrillation,  60,  62 

in  extrasystole,  54 


298 


INDEX 


Pulse  (Continued) 

pulsus  bigeminus,  48 

pulsus  celer,  20 

pulsus  durus,  20 

pulsus  magnus,  20 

pulsus  tardus,  20,  141 

soft,  20 

water-hammer,  20 
Pulse  Alternation 

description  of,  92 

digitalis  and,  206,  208 

mechanism  of,  92,  94 

method  of  estimating  blood  pressure  in, 
250 

occurrence  of,  92 
Pulsus    Alternans,  see  Pulse   Alterna- 
tion 
Pulsus  Paradoxus 

cardiac  palpation  in,  134 

mechanism  of,  92 
Purkinje  Fibers 

(see  also  Auriculo-ventricular  Con- 
duction SySTEM) 

distribution  of,  9 

excitation  wave  and,  44 
Pyogenic  Abcesses 

causing  endocarditis,  157 
Pyorrhea  Alveolaris 

cardiosclerosis  and,  157 

endocarditis  and,  156-157 

Q   Wave  of  Electrocardiogram 

cause  of,  26 

description  of,  26 

in  normal  electrocardiogram,  26 

origin  of,  in  heart,  42 

ventricular  motion  and,  35 
Q  R  S  Complex 

affected  by  ventricular  motion,  35 

cause  of,  27 

compared  to  M  and  W  waves,  35 

description  of,  26 

notched,  37 

prolonged,  36 

R  Wave 

cardiac  axis  and,  42 

description  of,  26 

in   asynchronous   ventricular   activity, 

35 
in  bundle-branch  lesions,  72 
in  drop  heart,  30 
in  heart  displacement,  30 
in  intraventricular  block,  36 
in  mitral  stenosis,  33 
in  nodal  extrasystole,  69 
in  squatty  heart,  28 
in  ventricular  extrasystole,  69 
in  ventricular  hypertrophy,  33 
interpretation  of,  27 
mathematical    principles    and    method 

of  determining,  39-43 


R  Wave  (Continued) 

phasic  variation  and,  32,  33 

variations  of  in  normal  electrocardio- 
gram, 26,  27 

wide,  36,  37,  38 
Radial  Pulse 

description  of,  18-20 

in  blood  pressure  estimation,  244 

palpation  of,  20 

types  of,  20 
Renal  Congestion 

in  chronic  endocarditis,  169 

phenolsulphophthalein  test  in,  231 
Respiration 

effect  on  a  waves,  64 

effect  on  position  of  heart,  32 

effect  on  pulse  beat,  92 

effect  on  systolic  pressure,  245 
Rest 

in  cardiac  disease,  223 

in  hypertension,  253 

in  rheumatic  endocarditis,  264 

in  senile  cardiosclerosis,  267 

in  "weak"  heart,  257 
Retinal  Hemorrhages 

in  streptococcus  viridans,  180 
Retinitis 

in  hypertension,  247,  262 
Rheumatism 

endocarditis  and,  165-167 

etiology  of,  151,  155,  157 

myocarditis  and,  155 

tonsillitis  and,  155 
Roentgenographs  Rays,  see  X-Ray 

jS   Wave  of  Electrocardiogram 

normal,  26 

significance  of,  42 

ventricular  motion  and,  35 
Salt 

in  nephritic  diet,  231,  233 
Salvarsan 

in  aneurismal  dilatation  of  aorta,  189, 
191,  192 

in  cardiac  syphilis,  184,  266 

in  luetic  heart  block,  101 
Secondary  Tidal  Wave,  19 
Semilunar  Valves 

cause    of    reduplicated    second    heart 
sound,  146 

in  cardiosclerosis,  164 

structure  of,  160 
Septum  Inferius,  1 
Septum  Superius,  1 
Serum,  Sensitized 

in  streptococcus  viridans  endocarditis, 
123,  182,  222 
Shock 

blood  pressure  in,  246 

strychnine  in,  219 
Sino-auricular    Block    (see   also   Heart 
Block) 

description  of,  82,  83 


INDEX 


299 


Sino-auricular  Block  (Continued) 

differentiation     of     blocked     auricular 
beat  from,  83 

differentiation     of     incomplete     heart 
block  from,  92 

due  to  smoking,  82,  83,  268 

etiology  of,  82,  97,  207 

tabulation,  48 

therapy  of,  97,  207 
Sino-auricular  Node 

blood  supply  of,  7 

center  of  excitation  wave,  44 

compared  with  auriculo-ventricular  con- 
duction system,  10 

disturbance    in,    causing    arrhythmias, 
48,  52,  79 

influence  of  neurogenic  and  myogenic 
impulses  on,  10 

mitral  stenosis  and,  104 

nerve  supply  of,  10,  259 

origin  of  normal  impulse  in,  10,  49 

position  of,  7 

structure  of,  7 
Sinus  Block,  see  Sino-auricular  Block 
Sinus  Reuniens  of  His,  see  Sinus  Veno- 

sus 
Sinus  Venosus 

development  of,  1 
Sleep 

diastolic  pressure  in,  245 
Sodium  Bicarbonate 

in  nephritic  acidosis,  233-234,  247 

in  uremia,  263 
Sodium    Nitrite 

in  hypertension,  252 
Spa  Treatment,  see  Baths 
Sparteine 

dose  of,  220 

effect  on  circulation,  220 
Sphygmogram,  see  also  Poltgraphic  Trac- 
ing 

definition  of,  12 
Sphygmomanometer 

aneroid,  243-245 

mercurial,  243-245 

method  of  use  of,  243-245 
Spleen 

in  chronic  rheumatic  endocarditis,  169 

in     streptococcus    viridans     infection, 
180 
Split  Complex 

cause  of,  34-35 
Squatty  Heart  (see  also  Orthodiascopy) 

cause  of,  28-30 

clinical  recognition  of,  28 

description  of,  28 
Squills,  Tincture  of 

heart  block  from,  216 

sinus  arrhythmia  from,  216 
Stimulation 

in  pneumonia,  273 
Streptococcus  Viridans 

blood  cultures  in,  181 


Streptococcus  Viridans  (Continued) 

blood  in,  179-180 

cardiac  symptoms  in,  180-181 

chronic  endocarditis  and,  175 

effect  of  silver  salts  on,  222-223 

effect  on  kidney,  178 

frequency  of  infection  from,  158 

nervous  manifestations  in,  180 

pathological  changes  in,  177-178 

petechise  in,  179 

pneumonic  complications  in,  180 

quiescent  interval  in,  181-182 

reinvasions  of,  181,  182 

serums  in,  182,  222 

skin  lesions  in,  179 

spleen  in,  180 

symptomatology  of  endocarditis  caused 
by,  167-172,  178,  179 

therapy  of,  182 

urine  in,  180 

vaccines  in,  182,  222 
Strophanthus 

in  pneumonia,  273 

use  of,  215 
Strophanthus,    Crystalline   (Strophan- 
thin) 

caution  in  using,  216 

compared  to  digitalis,  215—216 

dose  of,  215 

effect  on  ventricular  activity,  215 

in  auricular  fibrillation,  215 

in  cardiac  dyspnoea,  215 

in  cyanosis,  215 
Strychnine 

effect  on  blood  pressure,  219 

in  pneumonia,  273 
Stupor 

in  aortic  regurgitation,  173 

in     streptococcus     viridans     infection, 
180 
Substernal  Pains 

in    aneurismal    dilatation    of    descend- 
ing aorta,  189 
Sulphate  of  Magnesia,  221 
Summation  Wave,  54 
Suprarenal  Extract 

dose  of,  221 

effect  on  circulation,  220-221 

in  constitutional  hypotension,  221 

in  pneumonia,  273,  274 

in  "weak"  heart,  257 
Swallowing 

heart  block  and,  103 
Syphilis,  Cardiac,  see  Cardl\c  Syphilis 
Systole 

intensity  of,  4 

refractory  phase  of,  4 
Systolic  Pressure 

after  meals,  245-246 

as    test     of     cardiac     efficiency,    236- 
237 

diurnal  variations  of,  245 

maximal  normal,  245 


300 


INDEX 


Systolic  Pressure  (Continued) 

methods  of  determining,  244-245 
respiration  and,  245 

Systolic  Wave,  19 

T  Wave  of  Electrocardiogram 

auricular  extrasystoles  and,  52 

cause  of,  27,  42 

description  of,  26,  45 

diagnostic  significance  of,  45-46 

effect  of  digitalis  on,  45,  46,  274 

effect  of  exercise  on,  46 

negative,  45 

normal  variations  of,  26,  45,  46 
Tabagism 

blood  pressure  in,  246 

causing  auricular  fibrillation,  105,  268 

causing  auricular  flutter,  268 

causing  extrasystoles,  99,  269 

causing  sino-auricular  block,  82,  83,  97, 
268 

causing  tachycardia,  106 

endocarditis  and,  150,  151 

heart  block  and,  101 

precordial  pains  in,  268 

therapy  of  precordial  pains  in,  268 
Tabes 

precordial  pains  in,  271 
Tachycardia 

auricular,  68 

bromides  in,  221 

caused  by  tabagism,  151 

chest  palpation  in,  134 

differentiation  of   auricular  fibrillation 
from,  62 

functional  murmurs  in,  143 

hemoptyses     in     aortic     regurgitation 
with,  173 

in  acute  rheumatic  endocarditis,  264 

in  aortic  regurgitation,  173 

in  cardiosclerosis,  198,  202 

in  decompensated  mitral  stenosis,  170 

in  diphtheria,  152 

in  myocarditis,  174 

in  pregnancy  with  cardiac  lesions,  238 

inspection  of  apical  region  in,  131 

shortened  conduction  time  in,  104 

sino-auricular  block  and,  83 

therapy  of,  237 

ventricular  dilatation  from,  34 
Tachycardia,  Paroxysmal  Auricular 

classification,  47 

clinical  recognition  of,  55-56 

differentiation  of  paroxysmal  ventricu- 
lar from,  76 

electrocardiogram  of,  55 

etiology  of,  106 

in  acute  endocarditis,  166 

in  acute  indigestion,  106 

in  decompensated  mitral  stenosis,  172 

reduplicated    second    heart  sound    in, 
146 

shortened  conduction  time  in,  84 


Tachycardia,      Paroxysmal     Auricular 
(Continued) 

therapy  of,  106 

ventricular  rate  in,  55 
Tachycardia,  Paroxysmal  Ventricular 

clinical  characteristics  of,  76 

differentiation  of  paroxysmal  auricular 
from,  76 
Tachycardia,  Simple 

definition  of,  54,  55 

digitalis  in,  211-212 

diseases  accompanied  by,  106 

etiology  of,  106 

rate  in,  55,  106 

recognition  of,  55-56 

shortened  conduction  time  in,  84 

therapy  of,  106,  211-212 
Tea 

causing  extrasystoles,  99 

causing  tachycardia,  106 
Teeth,  Extraction  of 

in  endocarditis,  156-157,  227 
Teleroentgenography,  110 
Theobromine  Sodium  Salicylate 

advantages  over  caffein,  216-217 

causing  bradycardia,  78 

dose  of,  217 

effect  on  kidney,  217-218 

in  acute  rheumatic  endocarditis,    173, 
174 

in  cardio-renal  dropsy,  217 

in  cardiac  syphilis,  266 

in  cardiosclerosis,  267 

in  endo-myocardial  disease,  264 

intravenous  method  of  administration, 
217 

Murphy  drip  method  of  administering, 
217 

with  acetate  of  potash  and  soda,  221 

with  digitalis,  217 

with  Karrell  diet,  217-218 
Tone 

mechanism  of,  243-244 

relation  to  blood  pressure,  242-243 
Tonicity  of  Cardiac  Musculature,  4 
Tonsillectomy 

relation  to  endocarditis,  226-227 
Tonsillitis 

causing  endocarditis,  155—156 

relation  to  rheumatism,  155 
Toxins 

bradycardia  from,  99-100 

definition  of,  102,  152 

diphtheritic,  152-153 

extrasystoles  from,  98,  99 

fatty     degeneration     of     endocardium 
from,  160 

heart  block  from,  102 

in  pneumonia,  102,  274-276,  153-155 

in  pyogenic  abcesses,  157 

in  pyorrhea,  156-157 

in  tonsillitis,  155—156 

pneumonic,  153-155 


INDEX 


301 


Toxins  (Continued) 

premature  arteriosclerosis  from,  267 

rheumatic,  155 

ventricular  escape  and  rheumatic,  108 
Transudates,  Pleural 

in  chronic  endocarditis,  169 
Tricuspid  Valves 

ballooning  of,  17 

blood  vessels  in,  160 

frequency  of  bacterial  infection  of,  158 

in  tertiary  cardiac  syphilis,  184 

lesions  of,  141-142 

opening  of,  16 

position  of,  2 
Tumors 

causing  heart  block,  102 
Tumors,  Mediastinal 

causing  heart  displacement,  30 

causing  precordial  pains,  271 
Typhoid 

as  cause  of   endocarditis  and  myocar- 
ditis, 155 

U  Wave  of  Electrocardiogram 

description  of,  26 
Uremia 

blood  pressure  in,  247,  262 

in  prognosis  of  cardiosclerosis,  104 

precordial  pains  in,  262-263 

symptoms  of,  104,  247,  262-263 

theobromine  salicylate  soda  in,  217 

therapy  of,  263 

urine  in,  247,  262,  263 
Uric  Acid  in  Blood,  233 
Urine 

effect  of  caffein  on,  216 

effect  of  streptococcus  viridans,  180 

in  myocardial  insufficiency,  263 

in  nephritis,  233-234 

in  uremia,  247,  262,  263 

v  Wave 

divided,  16,  17 

in  auricular  fibrillation,  60 

normal,  16 

relation  to  dicrotic  notch,  19 
Vaccines 

autogenous,  123 

in  streptococcus  viridans,  182,  222 
Vagal  Inhibition 

caused  by  digitalis,  207 

caused  by  tincture  of  squills,  216 

causing  heart  block,  103 
Vagus 

cause  of  sino-auricular  block,  97,  207 

influence  on  rhythm,  50 

pressure  on,  causing  A-V  heart  block, 
102,  103 

relation    to    auriculo-ventricular   nerve 
supply,  10,  259 

relation  to  cardiac  energy,  242 

relation  to  premature  contractions,  97 

relation  to  sino-auricular  node,  7 


Vagus  (Continued) 

sino-auricular  block  and  the,  82,  207 

stimulation  of,  5 

tumors  and  adhesions  of,  102 
Valves    of    Heart    (see    also    Valvular 
Lesions) 

position  of,  2 

structure  of,  160 
Valvular  Lesions  (see  also  Mitral  and 
Aortic  Lesions,  and  Endocarditis) 

blood  pressure  in,  248 

exercise  in,  235 

marriage  of  women  with,  238 

relation  of  tonsillectomy  to,  227 

polygrams  of,  17 
Vasodilators,  252,  253,  261,  262 
Vasomotor  Mechanism 

effect  of  caffein  on,  216 

in  menopause,  270 

in  "weak"  heart,  255-257 
Venesection 

blood  pressure  and,  222,  246,  249,  252 

in  pneumonia,  274-275 
Venous  Polygraphic  Tracing,  see  Phle- 

BOGRAM 

Ventricle 

abnormal  mobility  of,  147 

abnormal  rocking  motion  of,  28,  34,  35, 
36,  q.v. 

abnormal   sequence  of   contraction  of, 
48 

change  of  position  of,  in  breathing,  32 

development  of,  1 

excitation  wave  in,  44,  45 

fibers  and  layers  of,  3 

in  drop  heart,  30 

in  fetal  heart,  2 

in  squatty  heart,  28 

nerve  supply  of,  5 

normal  impulse  in,  10 

normal  orthodiascopic  tracing  of,   111 

premature  contraction  of   (see  Extra- 
systole,  Ventricular) 

variation  in  contraction  time  of,  34,  35 
Ventricular  Arrhythmias 

cause  of,  68 

classification,  47 
Ventricular  Asynchronism 

description  of,  34-35 

M  and  W  waves  and,  35-36 

reduplicated  apical  impulse  and,  146 
Ventricular  Automatism,  see  Ventricu- 
lar Escape 
Ventricular      Complex      of      Electro- 
cardiogram 

cause  of,  26 

deviations  of,  26 
Ventricular  Contraction 

chest  palpation  and,  134 

effect  of  digitalis  on,  206 

effect  of  strophanthin  on,  216 

electrocardiographic  complex  of,  26 

in  "weak"  heart,  256 


302 


INDEX 


Ventricular  Contraction  {Continued) 

premature — (see  Extrasystole,  Ven- 
tricular) 

second  heart  sound  and,  147 
Ventricular  Diastole 

in  polygraphic  tracing,  16 
Ventricular  Dilatation,  28,  34 
Ventricular  Escape 

classification,  47 

description  of,  74-76 

etiology  of,  74,  76,  107-109 

murmurs  in,  108 
Ventricular  Fibrillation 

classification,  47 

digitalis  and,  203,  212-213 

in  cardiosclerosis,  203 

ventricular  arrhythmias  and,  68 
Ventricular  Hypertrophy 

acute  accidents  in  cardiosclerosis  and, 
203 

alcoholism  and,  150 

blood  pressure  in,  247 

causes  of,  33,  168 

chest  palpation  in,  134 

diagnosis  of,  33 

differentiation     of     aneurismal     aortic 
dilatation  from,  191 

differentiation  of  ventricular  dilatation 
from,  34 

digitalis  in,  214 

electrocardiogram     of     branch    lesions 
and,  77 

electrocardiographic  deviations  in,  33 

in  cardiosclerosis,  164 

in  prognosis  of  cardiosclerosis,  200 

length  of  life  in,  176,  200 

respiratory  phases  in,  32-33 

tricuspid  murmur  and,  142 

visible  epigastric  pulsations  in,  131,  132 
Ventricular  Hypertrophy,  Left 

aneurismal  aortic  dilatation  and,  190 

aortic  stenosis  and,  172 

apical  impulse  in,  147 

blood  pressure  in,  247 

cardiosclerosis  and,  164,  204-205 

clinical  evidences  of,  33 

heart  sounds  in,  204-205 

hypertension  with,  205,  247 

inspection  of  apical  region  in,  131 

physical  signs  of,  204-205 


Ventricular   Hypertrophy,    Left   (Con- 
tinued) 

reduplicated  apical  impulse  in,  146 

wide  R  wave  and,  37 
Ventricular  Hypertrophy,  Right 

apical  impulse  in,  205 

clinical  evidences  of,  33 

epigastric  pulsation  in,  205 

mitral  stenosis  and,  33 

physical  signs  of,  205 

pulmonic  sounds,  in,  205 
Ventricular  Incoordination 

causes  of,  76 

classification,  47 

types  of,  77 
Ventricular  Systole 

blood  pressure  and,  242 

differentiation     of     aortic     aneurismal 
pulsation  from,  133 

normal  jugular  pulse  and,  14,  15,  16 

relation  to  dicrotic  notch,  19,  20 

with  reduplicated  apical  impulse,  147 
Veronal 

in  endocarditis,  174 
Violet  Ray,  261 
Vocal  Cords 

paralysis  of,  in  mitral  stenosis,  170 
Vomiting 

"  caused  by  digitalis,  209-210 

in  cerebral  anemia,  249 

in  coronary  disease,  203 

in  uremia,  247,  262 

W   Complex 

abnormal  ventricular  mobility  and,  34 

clinical  significance  of,  35,  36 

cause  of,  34-35 
Walking 

as  exercise  in  cardiac  disease,  224,  236 

as  exercise  in  hypertension,  253 
"Weak"  Heart 

clinical  symptoms  of,  255-257 

fluoroscopy  in,  256 

misnomer,  115 

therapy  of,  257 

vasomotor  mechanism  in,  257 

X-Ray 

in  aneurismal  dilatation  of  the  aorta,  191 

orthodiascopy,  110,  111 

percussion  of  cardiac  outline  and,  137 


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